داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ دوره 69
ﺷﻤﺎره 7
ﻣﻬﺮ 1390
ﺻﺎﺣﺐ اﻣﺘﻴﺎز :داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ﻣﺪﻳﺮ ﻣﺴﺆول :دﻛﺘﺮ ﺳﻴﺪ ﺣﺴﻦ اﻣﺎﻣﻲرﺿﻮي ﺳﺮدﺑﻴﺮ :دﻛﺘﺮ ﻧﺎدره ﺑﻬﺘﺎش ﻣﺪﻳﺮ اﺟﺮاﻳﻲ :دﻛﺘﺮ ﻣﺤﻤﺪ ﻋﻠﻲ ﻧﻮﻳﺎن اﺷﺮف ﺷﻮراي دﺑﻴﺮان
دﻛﺘﺮ ﺷﺎﻫﻴﻦ آﺧﻮﻧﺪزاده ،دﻛﺘﺮ ﺻﺪﻳﻘﻪ ﺑﺮﻧﺎ ،دﻛﺘﺮ ﺟﻤﺸﻴﺪ ﺣﺎﺟﺘﻲ ،دﻛﺘﺮ ﻧﻴﻤﺎ رﺿﺎﻳﻲ ،دﻛﺘﺮ ﻧﮕﺎر ﺳﺠﺎدﻳﺎن ،دﻛﺘﺮ ﻋﻠﻲ ﻋﺮبﺧﺮدﻣﻨﺪ، دﻛﺘﺮ ﻧﻌﻤﺖاﷲ ﻋﻄﺎﻳﻲ ،دﻛﺘﺮ راﻣﺶ ﻋﻤﺮاﻧﻲﭘﻮر ،دﻛﺘﺮ ﻣﺤﻤﻮد ﻗﺎﺿﻲ ﺧﻮاﻧﺴﺎري ،دﻛﺘﺮ ﺳﻴﺪﺟﻮاد ﻗﺎﺿﻲ ﻣﻴﺮ ﺳﻌﻴﺪ ،دﻛﺘﺮ ﻣﻬﺮي ﻛﺪﺧﺪاﻳﻲ، دﻛﺘﺮ ﺳﻴﻨﺎ ﻣﺮادﻣﻨﺪ ،دﻛﺘﺮ زﻳﻨﺖ ﻧﺎدﻳﺎﺣﺘﻤﻲ ،دﻛﺘﺮ ﻣﺤﻤﺪ ﻋﻠﻲ ﻧﻮﻳﺎن اﺷﺮف ﻫﻴﺄت ﺗﺤﺮﻳﺮﻳﻪ
دﻛﺘﺮ ﻧﺎﺻﺮ اﺑﺮاﻫﻴﻤﻲ درﻳﺎﻧﻲ ،دﻛﺘﺮ ﻣﺤﻤﻮد اﻛﺒﺮﻳﺎن ،دﻛﺘﺮ ﻓﺮﻧﺎز آﻣﻮزﮔﺎر ﻫﺎﺷﻤﻲ ،دﻛﺘﺮ ﺑﺎﺑﻚ ﺑﻬﺎر ،دﻛﺘﺮ ﭘﺮوﻳﻦ ﭘﺎﺳﺎﻻر ،دﻛﺘﺮ ﭘﺮﻳﭽﻬﺮ ﭘﺎﺳﺒﺨﺶ، دﻛﺘﺮ زاﻫﺪ ﺣﺴﻴﻦ ﺧﺎن ،دﻛﺘﺮ زﻫﺮا ﺣﻼﺟﻲ ،دﻛﺘﺮ ﻓﺎﻃﻤﻪ داوري ﺗﻨﻬﺎ ،دﻛﺘﺮ ﻣﻬﺮﻧﺎز رﺳﻮﻟﻲﻧﮋاد ،دﻛﺘﺮ ﻣﺴﻌﻮد ﺳﺘﻮده ،دﻛﺘﺮ ﻋﻠﻴﺮﺿﺎ ﺷﻌﺒﺎﻧﻲ، دﻛﺘﺮ اﺣﻤﺪرﺿﺎ ﻃﻼﺋﻲﭘﻮر ،دﻛﺘﺮ ﻣﺤﻤﺪرﺿﺎ ﻇﻔﺮﻗﻨﺪي ،دﻛﺘﺮ ﻣﺤﻤﺪ ﻛﺠﺒﺎفزاده ،دﻛﺘﺮ ﺳﻴﺪ ﻣﺤﻤﺪﺟﻮاد ﻣﺮﺗﻀﻮي ،دﻛﺘﺮ اﻋﻈﻢاﻟﺴﺎدات ﻣﻮﺳﻮي، دﻛﺘﺮ ﻣﺤﻤﺪﺟﻮاد ﻣﻴﻜﺎﺋﻴﻠﻲ ،دﻛﺘﺮ ﺑﻬﺮوز ﻧﺒﺌﻲ ،دﻛﺘﺮ ﻣﺮﺿﻴﻪ وﺣﻴﺪ دﺳﺘﺠﺮدي ،دﻛﺘﺮ ﻣﺤﻤﺪرﺿﺎ ﻫﺎدﻳﺎن ﻫﻴﺄت ﺗﺤﺮﻳﺮﻳﻪ ﺑﻴﻦ اﻟﻤﻠﻠﻲ
دﻛﺘﺮ ﻓﺮﻫﻨﺎك اﺳﺪي )ﺷﻴﻜﺎﮔﻮ( ،دﻛﺘﺮ ﺟﻮاد ﭘﺮوﻳﺰي )ﻓﻴﻼدﻟﻔﻴﺎ( ،دﻛﺘﺮ ﻣﺤﻤﺪرﺿﺎ ﻛﺸﺘﮕﺮ )ﻟﻨﺪن( ،دﻛﺘﺮ اﻓﺸﻴﻦ ﮔﻨﺠﻲ )اﺳﺘﺮاﺳﺒﻮرگ(، دﻛﺘﺮ ﺷﻬﻼ ﻣﺴﻌﻮد )ﻓﻠﻮرﻳﺪا( ،دﻛﺘﺮ ﭘﺮوﻳﺰ ﻫﻨﺠﻨﻲ )ﭘﻨﺴﻴﻠﻮاﻧﻴﺎ( وﻳﺮاﺳﺘﺎران
دﻛﺘﺮ ﻧﺎدره ﺑﻬﺘﺎش ،دﻛﺘﺮ ﻣﺤﻤﺪ ﻋﻠﻲ ﻧﻮﻳﺎن اﺷﺮف ،دﻛﺘﺮ وﺣﻴﺪ ﻧﻴﻜﻮﻳﻲ ،دﻛﺘﺮ ﺳﻴﺪ ﺑﻬﻨﺎم ﻫﺎﺷﻤﻲ ﻫﻤﻜﺎران دﻓﺘﺮ ﻣﺠﻠﻪ
ﺣﺴﻴﻦ ﭼﺎﻳﭽﻲ ،راﺣﻠﻪ رﻣﻀﺎﻧﻲ ،ﺳﺤﺮ ﺻﺪﻳﻖ ،ﻣﻌﺼﻮﻣﻪ ﻋﺴﮕﺮي ،آرزو ﻛﻤﻴﺰاﻧﻲ ﻧﺸﺎﻧﻲ :ﺗﻬﺮان ،ﺧﻴﺎﺑﺎن ﻗﺪس ،ﺧﻴﺎﺑﺎن ﭘﻮرﺳﻴﻨﺎ ،داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،ﺳﺎﺧﺘﻤﺎن آﻣﻮزش ،ﻃﺒﻘﻪ اول ،ﺷﻤﺎره ،202دﻓﺘﺮ ﻣﺠﻠﻪ آدرس اﻟﻜﺘﺮوﻧﻴﻚ http://tumj.tums.ac.ir :ﭘﺴﺖ اﻟﻜﺘﺮوﻧﻴﻚmedjournal@tums.ac.ir : ﺻﻨﺪوق ﭘﺴﺘﻲ ،14155/6447ﺗﻠﻔﻜﺲOnline submission: http://journals.tums.ac.ir/login ، 88962510 : ﺑﺮاﺳﺎس ﻣﺼﻮﺑﻪ ﻛﻤﻴﺴﻴﻮن ﻧﺸﺮﻳﺎت ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﻛﺸﻮر ،ﺑﻪ ﻧﻮﻳﺴﻨﺪﮔﺎن ﻣﻘﺎﻻت اﻳﻦ ﻣﺠﻠﻪ اﻣﺘﻴﺎز ارﺗﻘﺎي ﻋﻠﻤﻲ ﭘﮋوﻫﺸﻲ ﺗﻌﻠﻖ ﻣﻲﮔﻴﺮد. ﺗﻴﺮاژ 1000 :ﻧﺴﺨﻪ
ﻟﻴﺘﻮﮔﺮاﻓﻲ ،ﭼﺎپ و ﺻﺤﺎﻓﻲ :ﺑﻬﺮﻧﮓ
)راﻳﮕﺎن(
ﻧﻤﺎﻳﻪ ﺷﺪه در:
SCOPUS, EMBASE, Cambridge Scientific Abstracts (CSA), CAB Abstracts (CABI), Chemical Abstract Service (CAS), DOAJ, Psych Info, ULRICH΄S, Index Copernicus, IMEMR, EMR Beta, SID, Magiran, Iran Medex
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان دوره 69
ﺷﻤﺎره 7
ﻣﻬﺮ 1390
ﻓﻬﺮﺳﺖ اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ زﻋﻔﺮان در ﻣﻘﺎﺑﻞ آﺳﻴﺐﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ در اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ -ﻣﻮﻗﺘﻲ در ﻣﻮش ﺻﺤﺮاﻳﻲ405.................................................................... .. ﻋﺎﺑﺪﻳﻦ وﻛﻴﻠﻲ ،ﻣﺤﻤﺪ رﺿﺎ ﻋﻴﻨﻌﻠﻲ ،اﺣﻤﺪ رﺿﺎ ﺑﻨﺪﮔﻲ
ﻣﻘﺎﻳﺴﻪ اﺛﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ در اﻟﻘﺎي زاﻳﻤﺎن در زﻧﺎن ﺑﺎ ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ413........................................................................... ﺷﻴﺮﻳﻦ ﻧﻴﺮوﻣﻨﺶ ،ﻣﻌﺼﻮﻣﻪ داداش ﻋﻠﻴﻬﺎ ،ﻣﻴﻨﺎ اﻛﺮﻣﻲ
ﻣﻘﺎﻳﺴﻪ دو روش ﺑﻲﺣﺴﻲ ﻧﺨﺎﻋﻲ در ﺣﺎﻟﺖﻫﺎي ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و ﻧﺸﺴﺘﻪ در ﺟﺮاﺣﻲ ﻋﺮوق اﻧﺪام ﺗﺤﺘﺎﻧﻲ420..................................................................... ..... ﻣﺤﻤﺪرﺿﺎ ﻣﻬﺎﺟﺮ ،ﻛﺴﺮي ﻛﺮوﻧﺪﻳﺎن ،زاﻫﺪ ﺣﺴﻴﻦﺧﺎن ،اﻓﺸﻴﻦ ﺟﻌﻔﺮزاده ،ﺳﻬﻴﻼ دﺑﻴﺮان
ﺗﺄﺛﻴﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ در زﻧﺎن ﺗﻤﺮﻳﻦ ﻛﺮده426......................................................................................................... اﻣﻴﺮ رﺷﻴﺪﻟﻤﻴﺮ ،ﻣﻬﺪﻳﻪ اﺑﺮاﻫﻴﻢﻧﻴﺎ ،ﻋﻠﻲ اﻛﺒﺮ ﻫﺎﺷﻤﻲ ﺟﻮاﻫﺮي
ﻣﻘﺎﻳﺴﻪ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل در ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ432....................................................................................................... ﻧﺴﺘﺮن ﺧﺴﺮوي ،ﻋﻠﻴﺮﺿﺎ اﻣﻴﻨﻴﺎن ،رﺿﺎ ﺗﻘﻲﭘﻮر
ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه :ﺑﺮرﺳﻲ 24ﺑﻴﻤﺎر438.............................................................................................................................................. رﺿﺎ ﺑﺎﻗﺮي ،ﻗﺪرت اﷲ ﻣﺪاح ،ﻋﻠﻴﺮﺿﺎ ﺗﻮﺳﻠﻲ ،ﻓﺎﻃﻤﻪ ﻧﻘﻮي رﻳﺎﺑﻲ
ﺑﺮرﺳﻲ ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﺎ ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ ﭘﺲ از ﻣﺪاﺧﻼت ﻛﺮوﻧﺮ در ﻣﺮﻛﺰ ﻗﻠﺐ و ﻋﺮوق ﺷﻬﻴﺪ رﺟﺎﻳﻲ ﺗﻬﺮان445................................................................. اﺣﻤﺪﻋﻠﻲ ﻳﻮﺳﻔﻲ ،ﻣﺤﺴﻦ ﻣﻌﺪﻧﻲ ،ﺣﻤﻴﺪرﺿﺎ ﻋﻈﻴﻤﻲ ،ﺣﺴﻴﻦ ﻓﺮﺷﻴﺪي
آﺗﺮزي ﻛﻮآن :ﺗﺠﺮﺑﻪ 13ﺳﺎﻟﻪ و ﺑﺮرﺳﻲ ﻣﺘﻮن :ﮔﺰارش ﻛﻮﺗﺎه451........................................................................................................................................ ﻣﺤﺴﻦ ﻧﺮاﻗﻲ ،ﻧﺎزﻧﻴﻦ ﺣﺠﺮاﻻﺳﻮدي
اﻧﺴﻴﺪاﻧﺲ ﺳﻨﺪروم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ ﺑﻌﺪ از ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ﺑﺎ ﻟﻴﺪوﻛﺎﻳﻴﻦ و ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ :ﺗﺎﺛﻴﺮ ﻧﻮع ﺳﻮزن و ﭘﻮزﻳﺸﻦ ﺟﺮاﺣﻲ :ﮔﺰارش ﻛﻮﺗﺎه453............................. ﻓﺮﻫﺎد اﻋﺘﻀﺎدي ،آﻳﻼر آﻫﻨﮕﺮي ،ﻫﺎﺟﺮ ﺷﻜﺮي ،ﻣﺤﻤﺪرﺿﺎ ﺧﺎﺟﻮي
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
راﻫﻨﻤﺎي ﻧﻮﻳﺴﻨﺪﮔﺎن -1اﺻﻮل ﻛﻠﻲ -1-1 :آﻳﻴﻦ ﻧﮕﺎرش زﺑﺎن ﻓﺎرﺳﻲ ﺑﻪﻃﻮر ﻛﺎﻣﻞ رﻋﺎﻳﺖ ﺷـﺪه و از
ﺳﻴﺎه و ﺳﻔﻴﺪ و دوﺑﻌﺪي ﺑﺎﺷﺪ و ﻋﻨﻮان ﺟﺪول ﺑﺎﻻي آن و در ﻧﻤـﻮدار زﻳـﺮ آن ﻗـﺮار
ﺑﻪﻛﺎر ﺑﺮدن ﻛﻠﻤﺎت ﺧﺎرﺟﻲ ﻛﻪ ﻣﻌﺎدلﻫﺎي دﻗﻴﻖ و رﺳﺎﻳﻲ در زﺑﺎن ﻓﺎرﺳﻲ دارﻧﺪ،
ﮔﻴﺮد )ﺑﺎ ذﻛﺮ ﺷﻤﺎره( .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻣﺤﺪودﻳﺖ ﺻﻔﺤﺎت ﻣﺠﻠﻪ ،ﺑﺪﻳﻬﻲ اﺳـﺖ از ﺗﻜـﺮار
ﺧﻮدداري ﺷﻮد -1-2 .ﻣﻘﺎﻻت ارﺳﺎﻟﻲ در ﭼﻬﺎر ﻧـﺴﺨﻪ )ﻳـﻚ ﻧـﺴﺨﻪ اﺻـﻞ و ﺳـﻪ
اراﻳﻪ ﻣﻄﺎﻟﺒﻲ ﻛﻪ در ﻣﺘﻦ آورده ﺷﺪهاﻧﺪ در ﺟـﺪاول و ﺑـﺎﻟﻌﻜﺲ ﺑﺎﻳـﺪ اﺟﺘﻨـﺎب ﻧﻤـﻮد،
ﻧﺴﺨﻪ ﻛﭙﻲ( ﺗﻬﻴﻪ و ﺗﺤﻮﻳﻞ دﻓﺘﺮ ﻣﺠﻠﻪ ﮔﺮدﻧـﺪ -1-3 .ﻣﻄﺎﻟـﺐ ﻣﻘﺎﻟـﻪ ﻓﻘـﻂ ﺑـﺮ روي
ﺟﺪاول و ﻧﻤﻮدارﻫﺎ ﻓﺎرﺳﻲ ﺑﺎﺷﻨﺪ .ﺑﺤﺚ -1 :آﺛﺎر و اﻫﻤﻴﺖ ﻳﺎﻓﺘﻪﻫﺎي ﺑﻪدﺳﺖ آﻣﺪه
ﻳﻚﻃﺮف ﻛﺎﻏﺬ A4و ﺑﻪﺻﻮرت ﻳﻚ ﺳﺘﻮﻧﻲ و ﻳﻚ ﺧﻂ درﻣﻴـﺎن ﺑـﺎ رﻋﺎﻳـﺖ ﺣﺎﺷـﻴﻪ
و ﻣﺤﺪودﻳﺖ آنﻫﺎ -2ذﻛﺮ ﻧﺘﺎﻳﺞ ﺗﺤﻘﻴﻖ ﻣـﺸﺎﺑﻪ دﻳﮕـﺮان و ذﻛـﺮ ﻣﻐـﺎﻳﺮات و ﻣـﻮارد
ﻻزم )ﺣﺪاﻗﻞ دو ﺳﺎﻧﺘﻲﻣﺘﺮ( ﺗﺎﻳﭗ ﮔﺮدﻧﺪ و ﻫﻤﻪ ﺻﻔﺤﺎت ﺷﻤﺎرهﮔﺬاري ﺷﻮﻧﺪ-1-4 .
ﻧﻘﺾﻛﻨﻨﺪه -3ﺗﻮﺿﻴﺢ ﻋﻠﺖ ﺗﻔﺎوت ﺑﻴﻦ ﻧﺘﺎﻳﺞ اﻳﻦ ﺗﺤﻘﻴﻖ ﺑﺎ ﺑﻘﻴﻪ -4ﺗﻮﺿـﻴﺢ ﻣـﻮارد
ﻣﻘﺎﻟﻪ ارﺳﺎﻟﻲ ﺑﻪﻃﻮر ﻫﻤﺰﻣﺎن ﺑﺮاي ﺳﺎﻳﺮ ﻣﺠﻼت ارﺳﺎل ﻧﮕﺮدد و در ﺳﺎﻳﺮ ﻣﺠﻼت
ﻛﺎرﺑﺮد ﻋﻤﻠﻲ و ﻗﺎﺑﻠﻴﺖ ﺗﻌﻤﻴﻢﭘﺬﻳﺮي ﻧﺘﺎﻳﺞ ﺑﻪدﺳﺖ آﻣـﺪه -5راﻫﻨﻤـﺎﻳﻲ ﺑـﺮاي اداﻣـﻪ
)ﺣﺘﻲ ﺑﻪ زﺑﺎن اﻧﮕﻠﻴﺴﻲ و ﻏﻴﺮه( ﺑﻪ ﭼﺎپ ﻧﺮﺳﻴﺪه ﺑﺎﺷﺪ -1-5 .ﻟـﻮح ﻓـﺸﺮده ﻣﻘﺎﻟـﻪ
ﺗﺤﻘﻴﻖ ﺧﻮد ﻳﺎ دﻳﮕﺮان ،در ﻣﺠﻤﻮع اراﻳﻪ آﻧﭽﻪ ﻛﻪ از اﻳﻦ ﺗﺤﻘﻴﻖ ﺑﻪ ﻋﻠﻢ اﺿـﺎﻓﻪ ﺷـﺪه
)ﺗﺮﺟﻴﺤﺎً ﺑﺎ ﺑﺮﻧﺎﻣﻪ Word 2003ﻳﺎ ﺑﺎﻻﺗﺮ( ﺑﺎ اﻋﻤﺎل آﺧﺮﻳﻦ اﺻﻼﺣﺎت ﻣﻮرد ﻧﻈﺮ ،ﭘﺲ
اﺳﺖ .ﻣﻨﺎﺑﻊ :ﺷﻤﺎره ﻣﻨﺎﺑﻊ ﺑﻪﻛﺎر ﮔﺮﻓﺘﻪ ﺷﺪه در ﻣﺘﻦ ﺑﺎﻳﺴﺘﻲ ﻗﻴﺪ ﺷﻮد و ﺑﻪﻃﻮر ﻗﻄﻌـﻲ
از درﻳﺎﻓﺖ ﻧﺎﻣﻪ ﭘﺬﻳﺮش ﻣﻘﺎﻟﻪ ،ﺑﻪ دﻓﺘﺮ ﻣﺠﻠﻪ اراﻳﻪ ﮔﺮدد -1-6 .ﻧﻮع ﻣﻘﺎﻻت ﭘﺬﻳﺮﻓﺘـﻪ
ﺑﺎﻳـﺪ از ﻋﺪد ﻳﻚ ﺷﺮوع و ﺑﻪﺗﺮﺗﻴـﺐ اﺿـﺎﻓﻪ ﮔـﺮدد .ﺿـﻤﻦ اﻧﻄﺒـﺎق ﻛﺎﻣـﻞ ﺗﻌـﺪاد
ﺷﺪه ﺷﺎﻣﻞ ﻣﻘﺎﻻت ﺗﺤﻘﻴﻘـﻲ ،ﻣﻘـﺎﻻت ﻣـﺮوري )از ﻧﻮﻳـﺴﻨﺪﮔﺎن ﺑـﺎ ﺗﺠﺮﺑـﻪ ﻛـﺎﻓﻲ و
رﻓﺮاﻧﺲﻫﺎي ﻣﺤﺘﻮاي ﻣﻘﺎﻟﻪ و ﻟﻴﺴﺖ اﻧﺘﻬﺎﻳﻲ آن ،ﻣﺘﻦ دﻗﻴﻖ رﻓﺮاﻧﺲﻫﺎ ﺑﻪﺗﺮﺗﻴﺐ ﻇﻬﻮر،
ﺻﺎﺣﺐ ﺗﺄﻟﻴﻔﺎت در ﻣﻮﺿﻮع ﻣﻘﺎﻟﻪ( و ﮔـﺰارش ﻣـﻮردي ﻣـﻲﺑﺎﺷـﺪ -1-7 .در اﻧﺠـﺎم
در ﻓﻬﺮﺳﺖ ﻣﻨﺎﺑﻊ آورده ﺷﻮﻧﺪ .ﻧﺤﻮه ﺗﻨﻈﻴﻢ ﻣﻨـﺎﺑﻊ ﺑـﻪ ﺷـﺮح ذﻳـﻞ ﻣـﻲﺑﺎﺷـﺪ .ﻣﻨـﺎﺑﻊ
ﭘﮋوﻫﺶ ،اﺻﻮل اﻋﻼﻣﻴﻪ ﻫﻠﺴﻴﻨﻜﻲ و ﺿﻮاﺑﻂ اﺧﻼق ﭘﺰﺷﻜﻲ رﻋﺎﻳﺖ ﮔﺮدد -2 .ﻧﺤﻮه
ﺑﻪﺻﻮرت ﻛﺘﺎب) :ﻧﺎمﺧﺎﻧﻮادﮔﻲ /ﻧﺎم ﻧﻮﻳﺴﻨﺪه /ﻓﺼﻞ /ﻋﻨﻮان /ﻓﺼﻞ /ﻋﻨﻮان ﻛﺘﺎب /ﻧـﺎم
ﺗﻨﻈﻴﻢ ﻣﻘﺎﻻت ﺗﺤﻘﻴﻘﻲ -2-1 :ﺻﻔﺤﻪ اول )ﺻﻔﺤﻪ ﻋﻨـﻮان( ﺑﺎﻳـﺴﺘﻲ ﺷـﺎﻣﻞ :ﻋﻨـﻮان
ﻧﻮﻳﺴﻨﺪﮔﺎن ﻛﺘﺎب /ﻧﺎم ﻧﺎﺷﺮ /ﻣﺤﻞ اﻧﺘﺸﺎر /ﺳﺎل /ﺻﻔﺤﺎت:
ﻣﻘﺎﻟﻪ ،ﻧﺎم و ﻧﺎمﺧﺎﻧﻮادﮔﻲ ﻧﻮﻳﺴﻨﺪﮔﺎن ،درﺟﻪ ﻋﻠﻤﻲ و آدرس دﻗﻴﻖ ﻛﻠﻴـﻪ ﻧﻮﻳـﺴﻨﺪﮔﺎن )از ﺟﻤﻠﻪ ﻛﺪ ﭘﺴﺘﻲ ،ﺗﻠﻔﻦ ،دورﻧﮕﺎر و (E-mailﻣﺤﻞ اﻧﺠﺎم ﭘﮋوﻫﺶ ،ﻣﺴﺌﻮل ﻣﻘﺎﻟﻪ و ﺗﺎرﻳﺦ ارﺳﺎل ﻣﻘﺎﻟﻪ ﺑﺎﺷﺪ -2-2 .ﺻﻔﺤﻪ دوم و ﺳﻮم ﺷﺎﻣﻞ ﺧﻼﺻﺔ ﻓﺎرﺳﻲ و اﻧﮕﻠﻴﺴﻲ و ﻛﻠﻤﺎت ﻛﻠﻴﺪي اﻧﮕﻠﻴﺴﻲ ﻣﻲﺑﺎﺷـﺪ .ﭼﻜﻴﺪه ﻣﻘﺎﻟﻪ ﻧﻤﻲﺑﺎﻳﺴﺖ از 250ﻛﻠﻤﻪ ﺑﻴـﺸﺘﺮ ﺑﺎﺷﺪ و در ﭼﻬﺎر ﭘﺎراﮔﺮاف ﺑﺎ ﻋﻨﺎوﻳﻦ زﻣﻴﻨـﻪ و ﻫـﺪف ،روش ﺑﺮرﺳـﻲ ،ﻳﺎﻓﺘـﻪﻫـﺎ،
Nochols DH, Randall CL. Massive eversion of the vagina. In: Nichols DH, Randall CL, editors. Vaginal Surgery. 3rd ed. Baltimore: Williams Wilkins; 1989. p. 328-57.
ﻣﻨﺎﺑﻊ ﺑﻪﺻﻮرت ﻣﻘﺎﻟﻪ) :ﻧﺎمﺧﺎﻧﻮادﮔﻲ( /ﻧﺎم /ﻋﻨﻮان ﻣﻘﺎﻟﻪ /ﻋﻨﻮان ﻛﺎﻣـﻞ ژورﻧـﺎل /ﺳـﺎل اﻧﺘﺸﺎر /ﺷﻤﺎره ﻣﺠﻠﻪ /ﺻﻔﺤﺎت .ﻣﺜﺎل .1 :ﻛﺎوﻳــﺎﻧﻲ ﺣــﺴﻴﻦ ،ﭘﻮرﻧﺎﺻــﺢ ﻣﻬﺮاﻧﮕﻴــﺰ. اﻋﺘﺒﺎرﻳﺎﺑﻲ و ﻫﻨﺠﺎرﺳﺎزي ﭘﺮﺳﺸﻨﺎﻣﻪ ﺳﺮﺷـﺖ و ﻣـﻨﺶ ﻛﻠـﻮﻧﻴﻨﺠﺮ TCIدر ﺟﻤﻌﻴـﺖ اﻳﺮاﻧﻲ .ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ1384 ،؛ ﺳﺎل ،63ﺷﻤﺎره :2ﺻﻔﺤﺎت 89ﺗﺎ .98
ﻧﺘﻴﺠﻪﮔﻴﺮي و ﻛﻠﻤﺎت ﻛﻠﻴﺪي )ﺣـﺪاﻗﻞ 3و ﺣـﺪاﻛﺜﺮ 7واژه( ﺳـﺎزﻣﺎﻧﺪﻫﻲ ﺷـﻮد.
ﻣﻘﺎﻟﻪ ﻧﺸﺮﻳﻪ در ﻧﺴﺨﻪ اﻟﻜﺘﺮوﻧﻴﻚ:
ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد ﻧﺴﺒﺖ 1-2-2-1در ﺗﻬﻴﻪ ﭼﻜﻴﺪه ﺑﺎ ﭼﻬﺎر ﻋﻨﻮان ﻓـﻮق ﻣـﻮرد ﻟﺤـﺎظ
CDI, Clinical Dermatology Illustrated [monograph on CD-ROM]. Reeves JRT, Maibach H. CMEA Multimedia Group, Producers. 2nd ed. Version 2.0 Scan Diego: CMEA; 1995.
ﻗﺮار ﮔﻴﺮد .ﭼﻜﻴﺪه اﻧﮕﻠﻴﺴﻲ ﺑﺎﻳﺪ ﻛـﺎﻣﻼ ﻣﻨﻄﺒـﻖ ﺑـﺎ ﭼﻜﻴـﺪه ﻓﺎرﺳـﻲ ﺑﺎﺷـﺪ و در ﺑﺨﺶﻫﺎي Conclusion ،Results ،Methods ،Backgroundو Keywords
-ﻋﻜﺲﻫﺎ ،ﻧﻤﻮدارﻫﺎ و ﺟﺪاول ﻣﺮﺑﻮط ﺑﻪ ﻣﻘﺎﻟﻪ ﺑﻪﻫﻤـﺮاه ﺗﻮﺿـﻴﺤﺎت آنﻫـﺎ ﺑﺎﻳـﺴﺘﻲ
ﺗﻬﻴﻪ ﮔﺮدد و در ﺣﺪود 230-250ﻛﻠﻤﻪ ﺑﺎﺷﺪ -2-3 .اﺻـﻞ ﻣﻘﺎﻟـﻪ ﺑﺎﻳـﺴﺘﻲ ﺷـﺎﻣﻞ
ﺟﺪاﮔﺎﻧﻪ و در دﻧﺒﺎﻟﻪ ﻣﺘﻦ اﺻﻠﻲ ﻣﻘﺎﻟـﻪ ) (textآورده ﺷـﻮد و ﺷـﻤﺎرهﮔـﺬاري ﮔـﺮدد.
ﻣﻮارد زﻳﺮ ﺑﺎﺷﺪ :ﻣﻘﺪﻣﻪ :ﻳﻚ ﺻﻔﺤﻪ ﺷﺎﻣﻞ -1 :اﻃﻼﻋﺎت ﻗﺒﻠﻲ و زﻣﻴﻨﻪاي اﻧﺠﺎم ﺷﺪه
ﻛﻴﻔﻴﺖ ﺗﺼﺎوﻳﺮ ارﺳﺎﻟﻲ ﺑﺎﻳﺪ ﻣﻄﻠﻮب ﺑﺎﺷﺪ .در اراﻳﻪ ﻋﻜﺲﻫﺎي اﺳﻜﻦ ﺷﺪه اﺳﺘﻔﺎده از
و ﺳﺎﺑﻘﻪ ﺑﺎ ذﻛﺮ رﻓﺮاﻧﺲ -2ﺿﺮورت اﻧﺠﺎم ﺗﺤﻘﻴﻖ -3ﺳﺆاﻻت ﺑﺪون ﭘﺎﺳﺨﻲ ﻛﻪ اﻳﻦ
رزوﻟﻮﺷﻦ ﺣﺪاﻗﻞ 600dpiﺿﺮوري اﺳﺖ .ﻋﻜﺲ ﻫﺎي ارﺳـﺎﻟﻲ ﺑﺎﻳـﺴﺘﻲ ﺑـﻪﺻـﻮرت
ﺗﺤﻘﻴﻖ ﺑﻪ آنﻫﺎ ﭘﺎﺳﺦ ﻣﻲﮔﻮﻳﺪ و ﺑﻴﺎن اﻳﻦ ﻣﻮﺿـﻮع ﻛـﻪ ﭼﮕﻮﻧـﻪ ﻧﺘـﺎﻳﺞ اﻳـﻦ ﺗﺤﻘﻴـﻖ
اﺻﻞ ﺑﺎﺷﺪ ،ﺑﻪ اﻧﻀﻤﺎم ﺳﻪ ﻧـﺴﺨﻪ ﻛﭙـﻲ رﻧﮕـﻲ و در ﭘـﺸﺖ ﻋﻜـﺲ ﺷـﻤﺎره آن ،ﻧـﺎم
ﻣﻲﺗﻮاﻧﺪ ﺑﻪ رﻓﻊ اﺑﻬﺎﻣﺎت ﻛﻤﻚ ﻛﻨﺪ -4 .ﺗﻌﺮﻳﻒ اﺻﻄﻼﺣﺎت ﺗﺨﺼﺼﻲ ﻳﺎ اﺧﺘﺼﺎرات
ﻧﻮﻳﺴﻨﺪه و ﺟﻬﺖ ﻧﺼﺐ ﺗﺼﻮﻳﺮ ﺛﺒﺖ ﮔﺮدد.
ﻋﻠﻤﻲ -6ﻫﺪف ﺗﺤﻘﻴﻖ ﺑﻪ ﻧﺤﻮ روﺷﻦ .روش ﺑﺮرﺳﻲ :ﺑﻪ ﻧﺤﻮي ﺑﺎﻳﺪ ﻧﻮﺷﺘﻪ ﺷﻮد ﻛﻪ
-3ﻧﺤﻮة ﺗﻨﻈﻴﻢ ﻣﻘﺎﻻت ﮔﺰارش ﻣﻮارد -3-ﺻﻔﺤﻪ اول ﺗﻮﺿﻴﺤﺎت اراﻳﻪ ﺷـﺪه در
ﻫﺮ ﺧﻮاﻧﻨﺪهاي ﺑﺘﻮاﻧﺪ ﺑﺎ آن ،ﺗﺠﺮﺑﻪ ﻧﻮﻳـﺴﻨﺪه ﻣﻘﺎﻟـﻪ را ﺗﻜـﺮار ﻛﻨـﺪ ،ﺷـﺎﻣﻞ :ﻃﺮاﺣـﻲ
ﻗﺴﻤﺖ -3-1 ،2-1ﺻﻔﺤﻪ دوم و ﺳﻮم ﺷﺎﻣﻞ ﺧﻼﺻﻪ ﻓﺎرﺳﻲ و اﻧﮕﻠﻴﺴﻲ و ﻛﻠﻤـﺎت
ﺗﺤﻘﻴﻖ :ﺟﺰﺋﻴﺎت روش ﻣﻄﺎﻟﻌﻪ و ﻋﻠﺖ اﻧﺘﺨﺎب آن )ﻣـﺜﻼ ﻛﻮﻫـﻮرت( -ﻣـﺪت زﻣـﺎن
ﻛﻠﻴﺪي اﻧﮕﻠﻴﺴﻲ ﻣﻲﺑﺎﺷﺪ .ﺧﻼﺻﻪ ﮔﺰارش ﻣﻮردي ﻧﺒﺎﻳـﺴﺘﻲ از 100ﻛﻠﻤـﻪ ﺑﻴـﺸﺘﺮ
اﺟﺮاي ﻃﺮح و ﭘﻲﮔﻴﺮي -1 .زﻣﺎن و ﻣﻜﺎن اﺟﺮاي ﭘﮋوﻫﺶ -2ﺳﻮژهﻫﺎ و ﻧﻤﻮﻧﻪﻫـﺎي
ﺑﺎﺷﺪ -3-3 .اﺻﻞ ﻣﻘﺎﻟﻪ ﺑﺎﻳﺴﺘﻲ ﺷﺎﻣﻞ ﻣﻮارد زﻳﺮ ﺑﺎﺷﺪ :ﻣﻘﺪﻣﻪ ،ﺷﺮح ﺣـﺎل ﺑﻴﻤـﺎر ﻳـﺎ
ﻣﻮرد آزﻣﻮن و ﻣﻼك اﻧﺘﺨﺎب .روش ﻧﻤﻮﻧﻪﮔﻴﺮي و ﻣﻨﻄﻖ ﺗﻌﺪاد ﻧﻤﻮﻧﻪ )اﻳـﻦ ﻗـﺴﻤﺖ
ﻣﻮرد ،ﺑﺤﺚ :ﮔﺰارش ﻣﻮرد و ﺑﺤﺚ ﻣﺠﻤﻮﻋﺎً از 1500ﻛﻠﻤﻪ ﺑﻴﺸﺘﺮ ﻧﺒﻮده و ﺣﺪاﻛﺜﺮ
ﺑﺴﻴﺎر ﻣﻬﻢ اﺳﺖ و در اﺑﺘﺪاي اﻣﺮ ﻣﻮرد ﻛﺎرﺷﻨﺎﺳﻲ ﻗﺮار ﻣﻲﮔﻴﺮد( -ﻣﻼكﻫﺎي ورود و
دو ﺟﺪول ﻳﺎ ﺗﺼﻮﻳﺮ اراﻳﻪ ﺷﻮد -3-4 .ﻣﻨﺎﺑﻊ ﻣﺸﺎﺑﻪ ﻣﻘﺎﻻت ﺗﺤﻘﻴﻘﻲ اﺳﺖ.
ﺧﺮوج ﺑﻪ ﻣﻄﺎﻟﻌﻪ -3 .ﻧﺤﻮه ﺟﻤﻊ آوري اﻃﻼﻋﺎت -4 .رﻋﺎﻳﺖ ﻣـﻮازﻳﻦ اﺧـﻼق در
-4ﻧﺤﻮه ﺗﻨﻈﻴﻢ ﻣﻘﺎﻻت ﻣـﺮوري -4-1 :اﻳـﻦ ﮔﻮﻧـﻪ ﻣﻘـﺎﻻت ﺑـﺮاي اراﻳـﻪ آﺧـﺮﻳﻦ
ﭘﮋوﻫﺶ -5اﺑﺰارﻫﺎي اﻧﺪازهﮔﻴﺮي -6آزﻣﻮنﻫﺎي آﻣﺎري -7ﻧﺎم ﻛـﺸﻮر و ﺷـﺮﻛﺖ
ﻳﺎﻓﺘﻪﻫﺎي ﻋﻠﻤﻲ درﺑﺎره ﻳﻚ ﻣﻮﺿﻮع ﺧﺎص ﺑﺎﺷﺪ -4-2 .ﻧﻮﻳﺴﻨﺪه در زﻣﻴﻨـﻪ ﻣﻮﺿـﻮع
ﺳﺎزﻧﺪه ﻣﻮاد و دﺳﺘﮕﺎهﻫﺎ .ﻳﺎﻓﺘﻪ ﻫﺎ :اراﻳـﻪ ﻧﺘـﺎﻳﺞ دﻗﻴـﻖ -1 :رﻋﺎﻳـﺖ اﺻـﻮل ﻋﻠﻤـﻲ
ﻣﻘﺎﻟﻪ ﻣﻲﺑﺎﻳﺴﺖ ﺻﺎﺣﺐ ﻧﻈﺮ و داراي ﻣﻘﺎﻟﻪ ﺑﺎﺷـﻨﺪ -5 .ﻫﻴـﺄت ﺗﺤﺮﻳﺮﻳـﻪ ﻣﺠﻠـﻪ در
)ﮔﺰارش ﻋﺪد ﺑﺎ درﺻﺪ -ﮔﺰارش ﻣﻴﺎﻧﮕﻴﻦ ﺑﺎ ﺣﺪود اﻃﻤﻴﻨـﺎن -ﻣﻴﺎﻧـﻪ ﺑـﺎ -2 (Range
ﻗﺒﻮل ﻳﺎ ﻋﺪم ﻗﺒﻮل و ﻳﺎ اﺻﻼح ﻣﻘﺎﻟﻪ )ﺑﺎ ﺗﺄﻳﻴﺪ ﻣﺆﻟﻒ( آزاد اﺳـﺖ و از ﭘـﺲ دادن
ﭘﺮﻫﻴﺰ از ﻧﺸﺎن دادن ﻫﻤﻪ ﻳﺎﻓﺘﻪﻫﺎي ﺑﻪدﺳﺖ آﻣﺪه ﺑﻪﺟﺰ ﻳﺎﻓﺘﻪﻫﺎي ﻣﻬﻢ و ﺗﻌﻴـﻴﻦﻛﻨﻨـﺪه
ﻣﻘﺎﻟﻪ و ﻣﻠﺤﻘﺎت آن ﻣﻌﺬور ﻣﻲﺑﺎﺷﺪ -6 .ﻧﻮﻳـﺴﻨﺪﮔﺎن ﻣﻘـﺎﻻت ﻣـﺴﺌﻮل ﻧﻮﺷـﺘﻪﻫـﺎ و
-3اﺳﺘﻔﺎده ﻣﻨﺎﺳﺐ از ﺟﺪول و ﻧﻤﻮدار ﺑﺎ ﺣﺪاﻗﻞ ﺗﻌﺪاد ﻣﻤﻜﻦ ﺑﻪﻃﻮريﻛﻪ ﺑـﻪ ازاي
ﻣﺪاﻓﻊ ﻣﻄﺎﻟﺐ ﭼـﺎپ ﺷـﺪه از ﻣﻘﺎﻟـﻪ ﺧـﻮد در ﻣﺠﻠـﻪ ﺧﻮاﻫﻨـﺪ ﺑـﻮد -7 .اﺳـﺘﻔﺎده از
ﻫﺮ ﺳﻪ ﺻﻔﺤﻪ ﺗﺎﻳﭙﻲ ﻳﻚ ﺟﺪول ﻳﺎ ﻧﻤﻮدار اﺳﺘﻔﺎده ﺷﻮد ،ﺿﻤﻦ اﻳﻦﻛﻪ ﻧﻤﻮدار ﺑﺎﻳـﺪ
ﻣﻨﺪرﺟﺎت ﻣﺠﻠﻪ ﺑﺎ ذﻛﺮ ﻛﺎﻣﻞ ﻣﺄﺧﺬ آزاد اﺳﺖ.
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
405-412 ،1390 ﺷﻤﺎره 7 دوره ، 69 ﻫﺎيﺗﻬﺮان، آﺳﻴﺐﻜﻲ ﻋﻠﻮم ﭘﺰﺷ ﻣﺤﺎﻓﻈﺘﻲداﻧﺸﮕﺎه اﺛﺮﭘﺰﺷﻜﻲ، ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﻣﻬﺮﻣﻮش ﻣﻐﺰي ،در اﻳﺴﻜﻤﻲ اﻛﺴﻴﺪاﺗﻴﻮ زﻋﻔﺮان در
اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ زﻋﻔﺮان در ﻣﻘﺎﺑﻞ آﺳﻴﺐﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ در اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ -ﻣﻮﻗﺘﻲ در ﻣﻮش ﺻﺤﺮاﻳﻲ
ﭼﻜﻴﺪه
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ﻋﺎﺑﺪﻳﻦ وﻛﻴﻠﻲ
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1390/04/21 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/05/03 :
زﻣﻴﻨﻪ و ﻫﺪف :ﻣﻄﺎﻟﻌﺎت ﻣﺘﻌﺪد ﻧﺸﺎن دادهاﻧﺪ زﻋﻔﺮان اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ در ﻣﻘﺎﺑﻞ آﺳﻴﺐ اﻛﺴﻴﺪاﺗﻴﻮ در اﻳﺴﻜﻤﻲ ﮔﻠﻮﺑﺎل
1
ﻣﺤﻤﺪ رﺿﺎ ﻋﻴﻨﻌﻠﻲ
ﻣﻐﺰي دارد ،اﻣﺎ اﺛﺮ آن ﺑﺮ ادم ﻣﻐﺰي و آﺳﻴﺐ اﻛﺴﻴﺪاﺗﻴﻮ در اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ ﻛﺎﻣﻼ ﻣﺸﺨﺺ ﻧﻴﺴﺖ .اﻳﻦ ﻣﻄﺎﻟﻌﻪ
2
اﺣﻤﺪ رﺿﺎ ﺑﻨﺪﮔﻲ
ﺑﺎ ﻫﺪف ﺑﺮرﺳﻲ اﺛﺮ زﻋﻔﺮان ﺑﺮ ادم ﻣﻐﺰي ،ﺣﺠﻢ ﺿﺎﻳﻌﺎت ﻣﻐﺰي و ﻣﻴﺰان ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢﻫﺎي آﻧﺘﻲ اﻛﺴﻴﺪاﻧﺖ )آﻧﺰﻳﻢ -1ﮔﺮوه ﻓﻴﺰﻳﻮﻟﻮژي ،ﻣﺮﻛﺰ ﺗﺤﻘﻴﻘﺎت و ﺑﺨﺶ
ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز و ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ( و ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻣﻐﺰ در ﻣﺪل ﺗﺠﺮﺑﻲ
ﻓﻴﺰﻳﻮﻟﻮژي
ﺳﻜﺘﻪ ﻣﻐﺰي ﻃﺮاﺣﻲ ﺷﺪ .روش ﺑﺮرﺳﻲ :اﻳﺴﻜﻤﻲ ﻣﻮﺿﻌﻲ ﺑﺎ ﻣﺴﺪود ﻛﺮدن ﻣﻮﻗﺘﻲ ﺷﺮﻳﺎن ﻣﻴﺎﻧﻲ ﻣﻐﺰ ﺑﺮاي ﻣﺪت ﻳﻚ
-2ﮔﺮوه ﺑﻴﻮﺷﻴﻤﻲ
ﺳﺎﻋﺖ در ﻣﻮش ﺻﺤﺮاﻳﻲ اﻳﺠﺎد ﺷﺪ .زﻋﻔﺮان ﺑﺎ دوز 100mg/kg ipدر ﺷﺮوع اﻳﺴﻜﻤﻲ ﺑﻪﺻﻮرت داﺧﻞ ﺻﻔﺎﻗﻲ ﺗﺰرﻳﻖ
داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺳﻤﻨﺎن،
و 24ﺳﺎﻋﺖ ﺑﻌﺪ ادم و ﺣﺠﻢ آﺳﻴﺐ ﻣﻐﺰي اﻧﺪازهﮔﻴﺮي ﺷﺪ .ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ و ﻣﻴﺰان ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢ ﺳﻮﭘﺮ
ﺳﻤﻨﺎن ،اﻳﺮان.
اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز و ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻣﻐﺰ ﺑﺎ اﺳﺘﻔﺎده از ﻛﻴﺖ ﻣﺨﺼﻮص اﻧﺪازهﮔﻴﺮي ﺷﺪ. ﻳﺎﻓﺘﻪﻫﺎ :زﻋﻔﺮان ﺣﺠﻢ ﺿﺎﻳﻌﺎت ﻣﻐﺰي را (P<0/001) %77و ادم ﻣﻐﺰي را (P<0/001) %60در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﮔﺮوه ﺷﺎﻫﺪ ﻛﺎﻫﺶ داد .ﻫﻤﻴﻦﻃﻮر زﻋﻔﺮان ﺑﻪﻃﻮر ﻣﻌﻨﻲداري ﻏﻠﻈﺖ ﺑﺎﻓﺘﻲ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ را ﻛﺎﻫﺶ داده ) (P<0/001و ﻣﻴﺰان ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢ ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز ) (P<0/001و ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ ) (P<0/001در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ﺑﻪﻃﻮر ﻣﻌﻨﻲداري اﻓﺰاﻳﺶ داد .ﻧﺘﻴﺠﻪﮔﻴﺮي :زﻋﻔﺮان اﺛﺮات ﻣﺤﺎﻓﻈﺘﻲ در ﻣﻘﺎﺑﻞ آﺳﻴﺐ اﻛﺴﻴﺪاﺗﻴﻮ اﻳﺴﻜﻤﻴﻚ و ادم
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ﻣﻐﺰي در ﻣﺪل اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ -ﻣﻮﻗﺘﻲ در ﻣﻮش ﺻﺤﺮاﻳﻲ دارد .اﻳﻦ اﺛﺮ اﺣﺘﻤﺎﻻ از ﻃﺮﻳﻖ اﻓﺰاﻳﺶ ﻇﺮﻓﻴﺖ ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﺳﻤﻨﺎن ،ﻛﻴﻠﻮﻣﺘﺮ 5ﺟﺎده داﻣﻐﺎن،
آﻧﺰﻳﻢﻫﺎي آﻧﺘﻲاﻛﺴﻴﺪان و ﻛﺎﻫﺶ ﺗﻮﻟﻴﺪ رادﻳﻜﺎلﻫﺎي آزاد اﻋﻤﺎل ﻣﻲﺷﻮد.
داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،ﻣﺮﻛﺰ ﺗﺤﻘﻴﻘﺎت و ﺑﺨﺶ ﻓﻴﺰﻳﻮﻟﻮژي ﺗﻠﻔﻦ0231-3354161 : E-mail: Abvakili@yahoo.com
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :زﻋﻔﺮان ،آﺳﻴﺐ اﻛﺴﻴﺪاﺗﻴﻮ ،اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ ،ادم ﻣﻐﺰي ،ﻣﻮش ﺻﺤﺮاﻳﻲ.
ﻣﻴﺘﻮﻛﻨﺪريﻫﺎ و آزاد ﺷﺪن ﻣﺤﺘﻮﻳﺎت آنﻫﺎ و ﺗﺴﺮﻳﻊ ﺗﻮﻟﻴﺪ رادﻳﻜﺎلﻫﺎي
ﻣﻘﺪﻣﻪ
آزاد ﻣﻲﺷﻮد 1.ﻛﺎﻫﺶ ﻓﻌﺎﻟﻴﺖ و ﻇﺮﻓﻴﺖ آﻧﺰﻳﻢﻫﺎي آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ و
اﻣﺮوزه ﻣﺸﺨﺺ ﺷﺪه اﺳﺖ اﺳﺘﺮسﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ ﻧﻘﺶ ﻣﺤﻮري در
اﻓﺰاﻳﺶ رادﻳﻜﺎلﻫﺎي آزاد ﻣﻨﺠﺮ ﺑﻪ وارد ﺷﺪن آﺳﻴﺐ ﺟﺪي ﺑﻪ اﺟﺰاي
ﭘﺎﺗﻮژﻧﺰ ﺑﻴﻤﺎريﻫﺎي ﻧﻮرودژﻧﺮاﺗﻴﻮ و ﻧﻮروﻟﻮژﻳﻚ ﻧﻈﻴﺮ ،آﻟﺰاﻳﻤﺮ،
ﺗﺸﻜﻴﻞدﻫﻨﺪه ﺳﻠﻮل ﻧﻈﻴﺮ ﻟﻴﭙﻴﺪﻫﺎ ،ﭘﺮوﺗﻴﻴﻦﻫﺎ و اﺳﻴﺪﻫﺎي ﻧﻮﻛﻠﻴﻴﻚ ﺷﺪه
ﺑﻪدﻧﺒﺎل ﺳﻜﺘﻪ ﻣﻐﺰي و ﻳﺎ
و در ﻧﻬﺎﻳﺖ ﺑﺎﻋﺚ ﻣﺮگ ﺳﻠﻮﻟﻲ ﻣﻲﮔﺮدد 1.ﺷﻮاﻫﺪ ﭘﮋوﻫﺸﻲ ﻧﺸﺎن
ﻗﻄﻊ ﺟﺮﻳﺎن ﺧﻮن ﺑﻪ ﻗﺴﻤﺘﻲ از ﻣﻐﺰ ،ﻏﻠﻈﺖ اﻛﺴﻴﮋن و ﻣﻮاد ﻣﺘﺎﺑﻮﻟﻴﻜﻲ
ﻣﻲدﻫﻨﺪ ،رادﻳﻜﺎلﻫﺎي آزاد ﻧﻘﺶ اﻧﻜﺎرﻧﺎﭘﺬﻳﺮي در ﺗﺸﻜﻴﻞ ،ﮔﺴﺘﺮش
2و1
ﭘﺎرﻛﻴﻨﺴﻮن ،ﺗﺮوﻣﺎ و ﺳﻜﺘﻪ ﻣﻐﺰي دارﻧﺪ.
5-7
ﺑﻪﺳﺮﻋﺖ در ﻧﻮاﺣﻲ اﻳﺴﻜﻤﻴﻚ ﻣﻐﺰ ﻛﺎﻫﺶ ﻳﺎﻓﺘﻪ و در ﻋﺮض ﭼﻨﺪ
ادم و ﺿﺎﻳﻌﺎت ﺛﺎﻧﻮﻳﻪ ﻣﻐﺰي ﭘﺲ از ﺳﻜﺘﻪ ﻣﻐﺰي دارﻧﺪ.
دﻗﻴﻘﻪ ﺑﻪ ﺳﻄﻮح ﻏﻴﺮ ﻗﺎﺑﻞ ﺗﺸﺨﻴﺺ ﻣﻲرﺳﻨﺪ 3.ﻛﺎﻫﺶ اﻛﺴﻴﮋن ﺑﺎﻓﺘﻲ در
اﺳﺘﻔﺎده از ﻣﻮاد و ﻳﺎ داروﻫﺎي ﮔﻴﺎﻫﻲ ﻛﻪ ﺧﺎﺻﻴﺖ آﻧﺘﻲاﻛﺴﻴﺪان ﻗﻮي
ﻧﺎﺣﻴﻪ اﻳﺴﻜﻤﻴﻚ ﻣﻐﺰ ،ﺳﺒﺐ اﺧﺘﻼل در ﻋﻤﻠﻜﺮد ﻣﻴﺘﻮﻛﻨﺪريﻫﺎ و ﺗﻮﻟﻴﺪ
داﺷﺘﻪ ﺑﺎﺷﺪ ،ﻣﻤﻜﻦ اﺳﺖ ﺑﺘﻮاﻧﺪ ﻣﻐﺰ را در ﻣﻘﺎﺑﻞ آﺳﻴﺐﻫﺎي ﻧﺎﺷﻲ از
رادﻳﻜﺎلﻫﺎي آزاد ﻣﻲﺷﻮد 4.از ﻃﺮﻓﻲ ﺑﺮﻗﺮاري ﻣﺠﺪد ﺟﺮﻳﺎن ﺧﻮن ﺑﻌﺪ
اﻛﺴﻴﺪاﻧﺖﻫﺎ در ﺳﻜﺘﻪ ﻣﻐﺰي ﺗﺎ ﺣﺪودي ﻣﺤﺎﻓﻈﺖ ﻧﻤﻮده و ﺑﺎﻋﺚ
از وﻗـﻮع ﺳﻜﺘﻪ ﻣﻐﺰي ﺳﺒﺐ اﻓﺰاﻳـﺶ ﺗﻮﻟﻴـﺪ ﭘﺮواﻛﺴﻴـﺪاﻧﺖﻫﺎ ،آﺳﻴـﺐ
ﻛﺎﻫﺶ ﻣﺮگ و ﻣﻴﺮ ﻧﺮوﻧﻲ ﺷﻮد .زﻋﻔﺮان ﺑﺎ ﻧﺎم ﻋﻤﻮﻣﻲ Saffronو ﻧﺎم
ﺑﻨﺎﺑﺮاﻳﻦ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻋﺎﺑﺪﻳﻦ وﻛﻴﻠﻲ و ﻫﻤﻜﺎران
406
ﻋﻠﻤﻲ Crocus Sativus L.از ﺧﺎﻧﻮاده زﻧﺒﻘﻴﺎن ) (Iridaceaeﮔﻴﺎﻫﻲ
وﻳﺴﺘﺎر ) 280-320ﮔﺮم( اﺳﺘﻔﺎده ﮔﺮدﻳﺪ .ﺣﻴﻮاﻧﺎت در ﺷﺮاﻳﻂ اﺳﺘﺎﻧﺪارد
ﻋﻠﻔﻲ ،ﭼﻨﺪ ﺳﺎﻟﻪ ،ﺑﺪون ﺳﺎﻗﻪ و ﭘﻴﺎزدار اﺳﺖ و ﺑﻪﻣﻴﺰان زﻳﺎد در ﻣﻨﺎﻃﻘﻲ
و دﺳﺘﺮﺳﻲ آزاد ﺑﻪ آب و ﻏﺬا ﻧﮕﻪداري ﺷﺪه و ﻛﻠﻴﻪ آزﻣﺎﻳﺸﺎت ﻣﻄﺎﺑﻖ
8
آﻳﻴﻦﻧﺎﻣﻪ ﻛﻤﻴﺘﻪ اﺧﻼق ﭘﮋوﻫﺸﻲ در ﻣﺮﻛﺰ ﺗﺤﻘﻴﻘﺎت ﻓﻴﺰﻳﻮﻟﻮژي داﻧﺸﮕﺎه
ﻧﻈﻴﺮ ﺳﻮاﺣﻞ ﻣﺪﻳﺘﺮاﻧﻪ ،اﻳﺮان ،ﻫﻨﺪ ،ﺗﺒﺖ ،ﭼﻴﻦ ،و ﻏﻴﺮه ﻛﺸﺖ ﻣﻲﺷﻮد.
زﻋﻔﺮان ﻋﻼوه ﺑﺮ اﻳﻦﻛﻪ ﻳﻚ ﭼﺎﺷﻨﻲ ﻏﺬاﻳﻲ ﭘﺮﻣﺼﺮف اﺳﺖ ،اﺛﺮات
ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺳﻤﻨﺎن در ﺳﺎل 1389اﻧﺠﺎم ﮔﺮدﻳﺪ.
ﻓﺎرﻣﺎﻛﻮﻟﻮژﻳﻜﻲ ﻣﺘﻌﺪدي ﻧﻴﺰ دارد 9.ﭘﮋوﻫﺶﻫﺎي ﺟﺪﻳﺪ ﻧﺸﺎن ﻣﻲدﻫﻨﺪ،
ﭘﺮوﺗﻜﻞ و ﻃﺮح آزﻣﺎﻳﺶ :آزﻣﺎﻳﺸﺎت ﻣﺮﺣﻠﻪ اول :ﺟﻬﺖ ارزﻳﺎﺑﻲ اﺛﺮ
زﻋﻔﺮان و ﻣﻮاد ﻣﻮﺛﺮه آن ،اﺛﺮات ﺿﺪ ﺗﻮﻣﻮري ،آﻧﺘﻲاﻛﺴﻴﺪان،
زﻋﻔﺮان ) (Sigma-Germanyﺑﺮ ﺿﺎﻳﻌﺎت ﻣﻐﺰي 21 ،ﺳﺮ ﻣﻮش
آﻧﺘﻲژﻧﻮﺗﻮﻛﺴﻴﻚ ،ﺗﻘﻮﻳﺖﻛﻨﻨﺪه ﺣﺎﻓﻈﻪ و ﻳﺎدﮔﻴﺮي ،ﺿﺪ درد و ﺿﺪ
ﺻﺤﺮاﻳﻲ ﺑﻪ ﺳﻪ ﮔﺮوه ﻫﻔﺖﺗﺎﻳﻲ ﺑﻪﺗﺮﺗﻴﺐ زﻳﺮ ﺗﻘﺴﻴﻢ ﺷﺪﻧﺪ .ﮔﺮوه
اﻟﺘﻬﺎب ،ﺿﺪ ﺗﺸﻨﺞ ،ﺿﺪ اﻓﺴﺮدﮔﻲ ،ﭘﺎﻳﻴﻦآورﻧﺪه ﻓﺸﺎر ﺧﻮن،
ﻛﻨﺘﺮل ﻛﺎذب ) :(Shamدر اﻳﻦ ﮔﺮوه ﻓﻘﻂ ﻋﻤﻞ ﺟﺮاﺣﻲ ﺻﻮرت ﮔﺮﻓﺘﻪ
اﻓﺰاﻳﺶدﻫﻨﺪه اﻛﺴﻴﮋنرﺳﺎﻧﻲ ﺑﺎﻓﺖﻫﺎ ،ﮔﺸﺎد ﻛﻨﻨﺪه ﺑﺮوﻧﺶ ،ﺿﺪ ﺳﺮﻓﻪ و
وﻟﻲ ﺷﺮﻳﺎن ﻣﻴﺎﻧﻲ ﻣﻐﺰ ﺑﺴﺘﻪ ﻧﻤﻲﺷﺪ .ﮔﺮوه ﻛﻨﺘﺮل اﻳﺴﻜﻤﻴﻚ :در اﻳﻦ
ﻏﻴﺮه دارد 9-11.ﻋﻼوه ﺑﺮ اﻳﻦ ،ﻳﺎﻓﺘﻪ آزﻣﺎﻳﺸﮕﺎﻫﻲ ﺟﺪﻳﺪ ﻧﺸﺎن داده اﺳﺖ،
ﮔﺮوه ﺳﺎﻟﻴﻦ ﺑﻪﻋﻨﻮان ﺣﻼل دارو ﺑﻼﻓﺎﺻﻠﻪ ﺑﻌﺪ از اﻟﻘﺎي اﻳﺴﻜﻤﻲ
زﻋﻔﺮان و ﻳﺎ ﻣﻮاد ﻣﻮﺛﺮه آن ﻣﻲﺗﻮاﻧﺪ ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻗﺎﺑﻞ ﺗﻮﺟﻪ
ﺑﻪﺻﻮرت داﺧﻞ ﺻﻔﺎﻗﻲ ﺗﺰرﻳﻖ ﺷﺪ .ﮔﺮوه درﻣﺎن :زﻋﻔﺮان ﺑﺎ دوز
13
100mg/kgﺑﻪﺻﻮرت داﺧﻞ ﺻﻔﺎﻗﻲ در ﺷﺮوع اﻳﺴﻜﻤﻲ ﺗﺰرﻳﻖ ﺷﺪ .در
ﻣﻲﺷﻮد .ﻣﻄﺎﻟﻌﺎﺗﻲ ﻛﻪ در راﺑﻄﻪ ﺑﺎ اﺛﺮ ﻋﺼﺎره ﺗﺎم
ﻫﻤﻪ اﻳﻦ ﮔﺮوهﻫﺎ 24ﺳﺎﻋﺖ ﺑﻌﺪ اﻳﺴﻜﻤﻲ ﻣﻴﺰان آﺳﻴﺐ ﻣﻐﺰي ﺑﺮرﺳﻲ و
12
آﺳﻴﺐﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻛﻠﻴﻪ، 14
ﻗﻠﺐ
15
و ﻣﻐﺰ
ﻋﻀﻠﻪ اﺳﻜﻠﺘﻲ،
زﻋﻔﺮان در اﻳﺴﻜﻤﻲ ﻣﻐﺰي اﻧﺠﺎم ﺷﺪه ﻣﺤﺪود ﺑﻮده و ﻋﻤﺪﺗﺎ ﺗﺎﺛﻴﺮ
اﻧﺪازهﮔﻴﺮي ﻣﻲﺷﺪ.
ﺗﺮﻛﻴﺒﺎت ﻓﻌﺎل آن در اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮرد ﻣﻄﺎﻟﻌﻪ ﻗﺮار ﮔﺮﻓﺘﻪ اﺳﺖ.
آزﻣﺎﻳﺸﺎت ﻣﺮﺣﻠﻪ دوم :ﺟﻬﺖ ارزﻳﺎﺑﻲ اﺛﺮ زﻋﻔﺮان ﺑﺮ ادم ﻣﻐﺰي 21
ﻳﺎﻓﺘﻪﻫﺎي ﺟﺪﻳﺪ ﻧﺸﺎن ﻣﻲدﻫﻨﺪ ،ﻣﻮاد ﻣﻮﺛﺮه زﻋﻔﺮان ﻣﺜﻞ ﺳﺎﻓﺮﻧﺎل،
ﺳﺮ ﻣﻮش ﺻﺤﺮاﻳﻲ ﺑﻪ ﺳﻪ ﮔﺮوه ﻫﻔﺖﺗﺎﻳﻲ ﺗﻘﺴﻴﻢ ﻣﻲﺷﺪﻧﺪ ﻛﻪ ﺷﺎﻣﻞ
ﻛﺮوﺳﻴﻦ ،ﭘﻴﻜﺮوﺗﻮﻛﺴﻴﻦ و ﺗﺮيﻛﺮوﺳﻴﻦ اﺛﺮات ﻣﺤﺎﻓﻈﺘﻲ در ﻣﻘﺎﺑﻞ
ﮔﺮوه ﻛﻨﺘﺮل ﻛﺎذب ) ،(Shamﮔﺮوه ﻛﻨﺘﺮل اﻳﺴﻜﻤﻴﻚ و ﮔﺮوه درﻣﺎن ﺑﺎ
آﺳﻴﺐ ﻧﺎﺷﻲ اﺳﺘﺮس اﻛﺴﻴﺪاﺗﻴﻮ در ﻣﺪل ﺗﺠﺮﺑﻲ اﻳﺴﻜﻤﻲ ﮔﻠﻮﺑﺎل 16و
زﻋﻔﺮان ﺑﻮد .اﻳﻦ ﻣﺮﺣﻠﻪ از آزﻣﺎﻳﺶ ﺷﺒﻴﻪ ﻣﺮﺣﻠﻪ ﻳﻚ ﺑﻮد ﺑﺎ اﻳﻦ ﺗﻔﺎوت
ﻣﻮﺿﻌﻲ و اﻳﺴﻜﻤﻲ در ﺷﺮاﻳﻂ 15In vitroدارد .ﺗﻨﻬﺎ ﻳﻚ ﭘﮋوﻫﺶ ﻧﺸﺎن
ﻛﻪ ﺑﻪﺟﺎي ﺿﺎﻳﻌﺎت ﻣﻐﺰي ،درﺻﺪ ﻣﺤﺘﻮاي آب ﻣﻐﺰ
(%water
داد ،ﺗﺠﻮﻳﺰ ﺧﻮراﻛﻲ زﻋﻔﺮان ﻫﻔﺖ روز ﻗﺒﻞ از اﻳﺠﺎد اﻳﺴﻜﻤﻲ ﻣﻐﺰي
) contentﻛﻪ ﺷﺎﺧﺼﻲ از ادم ﻣﻐﺰي اﺳﺖ ،ﻣﺤﺎﺳﺒﻪ و اﻧﺪازهﮔﻴﺮي ﺷﺪ.
ﻣﻮﺿﻌﻲ ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻣﺮگ ﻧﺮوﻧﻲ و اﻓﺰاﻳﺶ ﻇﺮﻓﻴﺖ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ ﻣﻐﺰ در ﻣﻮش ﺻﺤﺮاﻳﻲ ﻣﻲﺷﻮد.
11
آزﻣﺎﻳﺸﺎت ﻣﺮﺣﻠﻪ ﺳﻮم :ﺟﻬﺖ ﺑﺮرﺳﻲ اﺛﺮ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ زﻋﻔﺮان 21 ﺳﺮ ﻣﻮش ﺻﺤﺮاﻳﻲ ﺑﻪ ﺳﻪ ﮔﺮوه ﻫﻔﺖﺗﺎﻳﻲ ﺗﻘﺴﻴﻢ ﺷﺪﻧﺪ ﻛﻪ ﺷﺎﻣﻞ ﮔﺮوه
ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ ﻋﺼﺎره زﻋﻔﺮان ﻣﺤﺘﻮي ﻫﻤﻪ ﺗﺮﻛﻴﺒﺎت ﻓﻌﺎل و ﻣﻮاد
ﻛﻨﺘﺮل ﻛﺎذب ) ،(Shamﮔﺮوه ﻛﻨﺘﺮل اﻳﺴﻜﻤﻴﻚ و ﮔﺮوه درﻣﺎن ﺑﺎ زﻋﻔﺮان
ﻣﻮﺛﺮ اﺳﺖ ،اﺣﺘﻤﺎﻻ اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ و آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ آن ﺑﻴﺸﺘﺮ از ﻛﺎرﺑﺮد
ﺑﻮد .اﻳﻦ ﻣﺮﺣﻠﻪ از آزﻣﺎﻳﺶ ﺷﺒﻴﻪ ﻣﺮﺣﻠﻪ ﻳﻚ ﺑﻮد ﺑﺎ اﻳﻦ ﺗﻔﺎوت ﻛﻪ
ﻣﺠﺰاي ﺗﺮﻛﻴﺒﺎت ﻣﻮﺛﺮ آن در اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﺧﻮاﻫﺪ ﺑﻮد .از ﻃﺮﻓﻲ
ﻏﻠﻈﺖ ﺑﺎﻓﺘﻲ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ ) Malondialdehyde (MDAﺑﺎ اﺳﺘﻔﺎده
ﺗﺎﻛﻨﻮن ﺗﺎﺛﻴﺮ زﻋﻔﺮان و ﻣﻮاد ﻣﻮﺛﺮ آن ﺑﺮ ادم ﻣﻐﺰي ﻣﻮرد ﺗﺤﻘﻴﻖ و
از روش ﺗﻴﻮﺑﺎرﺑﻴﺘﻮرﻳﻚ اﺳﻴﺪ و ﺳﻄﺢ ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢﻫﺎي ﺳﻮﭘﺮ اﻛﺴﻴﺪ )(SOD
ﭘﮋوﻫﺶ ﻗﺮار ﻧﮕﺮﻓﺘﻪ اﺳﺖ .ﺑﻨﺎﺑﺮاﻳﻦ ،ﻣﻄﺎﻟﻌﻪ ﺣﺎﺿﺮ ﺑﺎ ﻫﺪف ﺑﺮرﺳﻲ اﺛﺮ
دﻳﺲﻣﻮﺗﺎز
زﻋﻔﺮان ﺑﺮ ادم ،ﻣﻴﺰان آﺳﻴﺐ ﻣﻐﺰي و ﻫﻤﻴﻦﻃﻮر ﺳﻄﺢ ﻓﻌﺎﻟﻴﺖ
ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ﺑﺎ اﺳﺘﻔﺎده از ﻛﻴﺖ ﻣﺨﺼﻮص
آﻧﺰﻳﻢﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ )آﻧﺰﻳﻢ ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز و ﮔﻠﻮﺗﺎﺗﻴﻮن
) Crumlin, UKاﻧﺪازهﮔﻴﺮي ﺷﺪ.
ﭘﺮاﻛﺴﻴﺪ( و ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻛﻮرﺗﻜﺲ ﻣﻐﺰي در ﻣﺪل ﺗﺠﺮﺑﻲ ﺳﻜﺘﻪ ﻣﻐﺰي ﻃﺮاﺣﻲ ﺷﺪ.
و ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ
)(GPX
و در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ
(Randox Laboratories,
اﻳﺠﺎد اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ :ﺟﻬﺖ اﻳﺠﺎد اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ -ﻣﻮﻗﺘﻲ ،اﺑﺘﺪا ﻣﻮشﻫﺎي ﺻﺤﺮاﻳﻲ ﺑﺎ ﺗﺰرﻳﻖ ﻛﻠﺮال ﻫﻴﺪرات ) (Fluka-Germanyﺑﺎ دوز ) (400mg/kg ipﺑﻴﻬﻮش ﻣﻲﺷﺪﻧﺪ .ﺑﻌﺪ از
روش ﺑﺮرﺳﻲ
اﻃﻤﻴﻨﺎن از ﻋﻤﻴﻖ ﺑﻮدن ﺑﻴﻬﻮﺷﻲ ،ﺟﻬﺖ ﺛﺒﺖ ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ ﻣﻐﺰ،
در اﻳـﻦ ﻣﻄﺎﻟﻌﻪ ﺗﺠﺮﺑﻲ از ﺗﻌﺪاد 63ﺳﺮ ﻣﻮشﻫﺎي ﺻﺤﺮاﻳـﻲ ﻧﺮ ﻧﮋاد
اﺑﺘﺪا ﭘﻮﺳﺖ ﻧﺎﺣﻴﻪ ﮔﻴﺠﮕﺎﻫﻲ زاوﻳﻪ ﺑﻴﻦ ﭼﺸﻢ و ﮔﻮش ﺣﻴﻮان ﺑﺮش
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
407
اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ زﻋﻔﺮان در آﺳﻴﺐﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ اﻳﺴﻜﻤﻲ ﻣﻐﺰي در ﻣﻮش
NIH Image analyzer
داده و ﻋﻀﻠﻪ ﮔﻴﺠﮕﺎﻫﻲ در ﻣﺤﻞ ﭼﺴﺒﻨﺪﮔﻲ ﺑﻪ اﺳﺘﺨﻮان ﺟﺪا ﻧﻤﻮده و
اﺳﺘﻔﺎده از ﻧﺮماﻓﺰار
ﺳﭙﺲ ﺑﺎ ﻛﻤﻚ ﻣﻴﻜﺮودرﻳﻞ ﺣﻔﺮهاي ﻛﻮﭼﻚ در ﺳﻄﺢ اﺳﺘﺨﻮان
ﻣﺤﺎﺳﺒﻪ ﺣﺠﻢ ،ﺳﻄﺢ ﺿﺎﻳﻌﻪ ﻣﻘﺎﻃﻊ در ﺿﺨﺎﻣﺖ ﺑﺮش ﺿﺮب ﺷﺪ.
ﮔﻴﺠﮕﺎﻫﻲ اﻳﺠﺎد ﺷﺪ .ﺳﭙﺲ ﺑﺮاي اﻳﺠﺎد اﻳﺴﻜﻤﻲ ﻣﻮﺿﻌﻲ ﻣﻐﺰ ،در زﻳﺮ
ﺣﺠﻢ ﻛﻞ ﺿﺎﻳﻌﻪ ﻣﻐﺰي ﻧﻴﺰ از ﺣﺎﺻﻞ ﺟﻤﻊ ﺿﺎﻳﻌﺎت در ﻫﻔﺖ ﺑﺮش
ﻣﻴﻜﺮوﺳﻜﻮپ ﺑﺮﺷﻲ ﺑﻪﻃﻮل دو ﺳﺎﻧﺘﻲﻣﺘﺮ در ﺟﻠﻮ ﮔﺮدن ﺣﻴﻮان اﻳﺠﺎد
ﻣﻐﺰي ﺑﻪدﺳﺖ ﻣﻲآﻣﺪ.
اﻧﺪازهﮔﻴﺮي ﺷﺪ .ﺑﺮاي
18
و ﻋﻀﻼت اﻳﻦ ﻧﺎﺣﻴﻪ ﻛﻨﺎر زده ﺷﺪه و ﺷﺮﻳﺎنﻫﺎي ﻛﺎروﺗﻴﺪ ﻣﺸﺘﺮك و
ارزﻳﺎﺑﻲ ادم ﻣﻐﺰي :ﺣﺪود 24ﺳﺎﻋﺖ ﺑﻌﺪ از اﻳﺴﻜﻤﻲ ﺣﻴﻮان ﻛﺸﺘﻪ
ﺷﺎﺧﻪﻫﺎي آن ﻛﺎروﺗﻴﺪ ﺧﺎرﺟﻲ و داﺧﻠﻲ را از ﺑﺎﻓﺖ ﻫﻢﺑﻨﺪ و ﻋﺼﺐ
ﺷﺪه و ﻣﻐﺰ ﺑﻪدﻗﺖ ﺧﺎرج ﻣﻲﮔﺮدد .ﺳﭙﺲ ﭘﻴﺎز ﺑﻮﻳﺎي و ﭘﻞ ﻣﻐﺰي را
ﺟﺪا و اﻳﺰوﻟﻪ ﺷﺪ .ﺷﺎﺧﻪﻫﺎي ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ ﺧﺎرﺟﻲ ﺑﺎ اﺳﺘﻔﺎده از
ﺟﺪا ﻧﻤﻮده و ﻧﻴﻢﻛﺮه اﻳﺴﻜﻤﻴﻚ و ﺳﺎﻟﻢ ﻣﻐﺰ را ﺑﺎ ﻛﻤﻚ
Brain matrix
دﺳﺘﮕﺎه ﻛﻮﺗﺮي ﺟﻬﺖ ﺟﻠﻮﮔﻴﺮي از ﺧﻮنرﻳﺰي ﺳﻮزاﻧﺪه و ﻣﺴﺪود ﺷﺪ.
و ﺑﺎ دﻗﺖ ﺑﺴﻴﺎر زﻳﺎد ﺟﺪا ﻧﻤﻮده و وزن ﻣﺮﻃﻮب دو ﻧﻴﻢﻛﺮه ﺑﻪوﺳﻴﻠﻪ
در اداﻣﻪ ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ ﺧﺎرﺟﻲ و ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ ﻣﺸﺘﺮك ﺑﻪﺻﻮرت
ﺗﺮازوي دﻗﻴﻖ ﺑﻪدﺳﺖ ﻣﻲآﻳﺪ .در اداﻣﻪ ﺟﻬﺖ ﺑﻪدﺳﺖ آوردن وزن
داﻳﻤﻲ و ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ داﺧﻠﻲ ﺑﻪوﺳﻴﻠﻪ ﻣﻴﻜﺮوﻛﻼﻣﭗ ﺑﻪﻃﻮر ﻣﻮﻗﺖ
ﺧﺸﻚ ﻫﺮ ﻧﻴﻢﻛﺮه آنﻫﺎ را در داﺧﻞ Ovenﺑﺎ درﺟﻪ ﺣﺮارت 110 C
ﻣﺴﺪود ﻣﻲﺷﺪ .ﺳﭙﺲ ﻧﺦ ﻧﺎﻳﻠﻮن ﺑﺎ ﺷﻤﺎره 3/0ﻛﻪ ﻧﻮك آن ﺟﻠﻮ ﺷﻌﻠﻪ
ﺑﺮاي ﻣﺪت 24ﺳﺎﻋﺖ ﻗﺮار داده ﺷﺪ .در ﻧﻬﺎﻳﺖ در ﺻﺪ ﻣﺤﺘﻮاي آب
ﮔﺮده ﺷﺪه ﺑﻮد را از ﻃﺮﻳﻖ ﺑﺮﺷﻲ ﻛﻮﭼﻚ ﻛﻪ در ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ ﺧﺎرﺟﻲ اﻳﺠﺎد ﮔﺮدﻳﺪه وارد ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ داﺧﻠﻲ ﻣﻲﺷﺪ .ﺑﻌﺪ از اﻳﻦ
ﻣﻐﺰ ﻛﻪ ﺷﺎﺧﺺ ﻣﻴﺰان ادم ﻣﻐﺰي اﺳﺖ ﺑﺎ ﻓﺮﻣﻮل زﻳﺮ ﺑﻪدﺳﺖ آﻣﺪ. × 100
اﺧﺘﻼف وزن ﻣﺮﻃﻮب و ﺧﺸﻚ ﻧﻴﻢﻛﺮه
19
= %ﻣﺤﺘﻮاي آب ﻣﻐﺰ
وزن ﻣﺮﻃﻮب ﻧﻴﻢﻛﺮه
ﻣﺮﺣﻠﻪ ﭘﺮوب ﺟﺮﻳﺎنﺳﻨﺞ ﻟﻴﺰري در ﻣﺤﻞ ﺧﻮد در اﺳﺘﺨﻮان ﮔﻴﺠﮕﺎﻫﻲ ﺛﺎﺑﺖ ﺷﺪه و ﺟﺮﻳﺎن ﺧﻮن ﭘﺎﻳﻪ ﻣﻐﺰ ﺑﺮاي 15دﻗﻴﻘﻪ ﺛﺒﺖ ﻣﻲﺷﺪ ،ﺑﻌﺪ از
اﻧﺪازهﮔﻴﺮي ﺳﻄﺢ ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢ ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز و ﮔﻠﻮﺗﺎﺗﻴﻮن
ﺗﺜﺒﻴﺖ ﺟﺮﻳﺎن ﺧﻮن ،ﻧﺦ ﻧﺎﻳﻠﻮن داﺧﻞ ﺷﺮﻳﺎن ﻛﺎروﺗﻴﺪ داﺧﻠﻲ ﺑﻪآراﻣﻲ
ﭘﺮاﻛﺴﻴﺪ و ﺗﻌﻴﻴﻦ ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻣﻐﺰي:
ﺑﻪداﺧﻞ ﻣﻐﺰ ﻫﺪاﻳﺖ ﻣﻲﺷﺪ ﺗﺎ ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ ﺑﻪ ﻛﻤﺘﺮ از %15ﺗﺎ
ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ از اﻳﺴﻜﻤﻲ ﻣﻐﺰي ،ﺣﻴﻮان ﺗﺤﺖ ﺑﻴﻬﻮﺷﻲ
%20ﻣﻴﺰان ﭘﺎﻳﻪ ﻛﺎﻫﺶ ﻳﺎﺑﺪ 17.ﻳﻚ ﺳﺎﻋﺖ ﺑﻌﺪ از اﻳﺴﻜﻤﻲ ﻧﺦ ﻧﺎﻳﻠﻮن
ﻋﻤﻴﻖ ﻛﺸﺘﻪ و ﻣﻐﺰ ﺧﺎرج ﺷﺪه و ﻛﻮرﺗﻜﺲ از ﺑﻘﻴﻪ ﻗﺴﻤﺖﻫﺎي ﻣﻐﺰ ﺑﺎ
ﺑﻪآراﻣﻲ ﺧﺎرج و ﺟﺮﻳﺎن ﺧﻮن ﻣﺠﺪد ﺑﺮاي 23ﺳﺎﻋﺖ در ﺷﺮﻳﺎن ﻣﻴﺎﻧﻲ
دﻗﺖ ﺟﺪا ﺷﺪه و در ﻇﺮف ﻣﺨﺼﻮص در دﻣﺎي -70 Cﺗﺎ زﻣﺎن اﻧﺠﺎم
ﻣﻐﺰ ﺑﺮﻗﺮار ﻣﻲﺷﺪ .در ﻃﻮل ﻳﻚ ﺳﺎﻋﺖ اﻳﺴﻜﻤﻲ و ﺗﺎ 15دﻗﻴﻘﻪ ﺑﻌﺪ از
آزﻣﺎﻳﺶ ﻧﮕﻪداري ﻣﻲﺷﺪ .ﻧﻤﻮﻧﻪﻫﺎ در ﻫﻨﮕﺎم آزﻣﺎﻳﺶ در ﺑﺎﻓﺮ G
ﺧﺎرج ﻛﺮدن ﻧﺦ و ﺑﺮﻗﺮاري ﻣﺠﺪد ﺟﺮﻳﺎن ﺧﻮن ،ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ
ﻣﺨﺼﻮص ﻫﻤﻮژﻧﻴﺰه و در
ﺗﻮﺳﻂ دﺳﺘﮕﺎه ﺟﺮﻳﺎنﺳﻨﺞ ﻟﻴﺰري ﻫﺮ ﭘﻨﺞ دﻗﻴﻘﻪ ﺛﺒﺖ و ﻳﺎدداﺷﺖ
ﻣﺤﻠﻮل روﻳﻲ ) (Supernatantﻧﻤﻮﻧﻪ ﺟﻬﺖ اﻧﺪازهﮔﻴﺮي ﻓﻌﺎﻟﻴﺖ
ﻣﻲﺷﺪ 17.در ﺿﻤﻦ درﺟﻪ ﺣﺮارت ﺣﻴﻮان از ﻃﺮﻳﻖ رﻛﺘﺎل ﻛﻨﺘﺮل و در
آﻧﺰﻳﻢﻫﺎي SODو ،GPXﺗﻌﻴﻴﻦ ﻏﻠﻈﺖ MDAو ﭘﺮوﺗﻴﻴﻦ اﺳﺘﻔﺎده ﺷﺪ.
ﺗﻤﺎم ﻃﻮل ﻣﺪت ﺟﺮاﺣﻲ ﺗﺎ ﺑﻪﻫﻮش آﻣﺪن ﻛﺎﻣﻞ ﺣﻴﻮان در ﻣﺤﺪوده ﻓﻴﺰﻳﻮﻟﻮژﻳﻚ ﻧﮕﻪ داﺷﺘﻪ ﻣﻲﺷﺪ. ﺗﻌﻴﻴﻦ ﺣﺠﻢ ﺿﺎﻳﻌﻪ ﻣﻐﺰي :ﺗﺤﺖ ﺑﻴﻬﻮﺷﻲ ﻋﻤﻴﻖ ﺣﻴﻮان ﻛﺸﺘﻪ و
20000ﺳﺎﻧﺘﺮﻳﻔﻮژ ﺷﺪﻧﺪ .ﺳﭙﺲ از
ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢﻫﺎي ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪاز و ﺳﻮﭘﺮاﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز و ﺑﺎ اﺳﺘﻔﺎده از ﻛﻴﺖﻫﺎي ﺷﺮﻛﺖ راﻧﺪوﻛﺲ )UK
(Randox Laboratories,
Crumlin,و ﺑﺮ اﺳﺎس دﺳﺘﻮراﻟﻌﻤﻞ ﺷﺮﻛﺖ ﺳﺎزﻧﺪه و ﺑﺎ ﻛﻤﻚ
ﺳﺮش ﺟﺪا و ﻣﻐﺰ ﺧﺎرج ﺷﺪ .ﺑﺮاي ﺑﺮش ﮔﻴﺮي ،ﻣﻐﺰ را ﺑﻪﻣﺪت ﭘﻨﺞ
دﺳﺘﮕﺎه ﻓﺘﻮﻣﺘﺮ ) (Stat fax 3300-USAاﻧﺪازهﮔﻴﺮي ﮔﺮدﻳﺪ 20.ﺑﺮاي ﺗﻌﻴﻴﻦ
دﻗﻴﻘﻪ در ﻣﺤﻠﻮل ﺳﺮم ﻓﻴﺰﻳﻮﻟﻮژي ﭼﻬﺎر درﺟﻪ ﻗﺮار داده ،ﺳﭙﺲ ﺑﻪﻛﻤﻚ
ﻏﻠﻈﺖ ﭘﺮوﺗﻴﻴﻦ از روش ﺑﺮادﻓﻮرد اﺳﺘﻔﺎده ﺷﺪ 20 .ﺑﺮاي اﻳﻦ ﻣﻨﻈﻮر دو
Brain matrixﻫﻔﺖ ﺑﺮش ﺑﻪﻗﻄﺮ دو ﻣﻴﻠﻲﻣﺘﺮ از ﻣﻐﺰ ﺗﻬﻴﻪ ﻣﻲﮔﺮدﻳﺪ.
ﻣﻴﻠﻲﻟﻴﺘﺮ از ﻣﺤﻠﻮل ﺑﺮادﻓﻮرد ﺑﻪ 40ﻣﻴﻜﺮوﻟﻴﺘﺮ از ﻣﺤﻠﻮل ﻫﻤﻮژﻧﻴﺰه
ﺟﻬﺖ رﻧﮓآﻣﻴﺰي ،ﺑﺮشﻫﺎ را ﺑﻪﻣﺪت 15دﻗﻴﻘﻪ در ﻣﺤﻠﻮل دو درﺻﺪ
ﻧﻤﻮﻧﻪ ﺑﺎﻓﺘﻲ اﺿﺎﻓﻪ ﺷﺪه و ﺑﻪﻣﺪت ﭘﻨﺞ دﻗﻴﻘﻪ در دﻣﺎي آزﻣﺎﻳﺸﮕﺎه اﻧﻜﻮﺑﻪ
ﺗﺮيﻓﻨﻴﻞ ﺗﺘﺮازوﻟﻴﻮم ﻛﻠﺮاﻳﺪ ) (Sigma-Germanyﻗﺮار داده ﺷﺪ .در اﻳﻦ
ﺷﺪ .ﺳﭙﺲ در ﻃﻮل ﻣﻮج 595ﻧﺎﻧﻮﻣﺘﺮ و در ﺑﺮاﺑﺮ ﺑﻼﻧﻚ ﻣﻌﺮف ﺟﺬب
روش رﻧﮓآﻣﻴﺰي ﻣﻨﻄﻘﻪ ﺿﺎﻳﻌﻪ دﻳﺪه ﺑﻪ رﻧﮓ ﺳﻔﻴﺪ و ﻣﻨﻄﻘﻪ ﻧﺮﻣﺎل ﻣﻐﺰ
آن ﻗﺮاﺋﺖ ﺷﺪ .ﻣﻨﺤﻨﻲ اﺳﺘﺎﻧﺪارد ﺑﺎ اﺳﺘﻔﺎده از ﺳﺮم آﻟﺒﻮﻣﻴﻦ ﮔﺎوي رﺳﻢ
ﺑﻪ رﻧﮓ ﻗﺮﻣﺰ آﺟﺮي در ﻣﻲآﻳﺪ 18.در ﭘﺎﻳﺎن ﺑﺎ دورﺑﻴﻦ دﻳﺠﻴﺘﺎﻟﻲ از
و ﻏﻠﻈﺖ ﭘﺮوﺗﻴﻴﻦ ﺑﺎﻓﺖ ﺑﺮ اﺳﺎس آن اﻧﺪازهﮔﻴﺮي ﮔﺮدﻳﺪ .از روش
ﺑﺮشﻫﺎ ﻋﻜﺲ ﮔﺮﻓﺘﻪ و ﺑﻪ ﻛﺎﻣﭙﻴﻮﺗﺮ ﻣﻨﺘﻘﻞ و ﺳﻄﺢ ﻧﺎﺣﻴﻪ ﺿﺎﻳﻌﻪ دﻳﺪه ﺑﺎ
ﺗﻴﻮﺑﺎرﺑﻴﺘﻮرﻳﻚ اﺳﻴﺪ ﺑﺮاي اﻧﺪازه ﻏﻠﻈﺖ ﺑﺎﻓﺘﻲ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ اﺳﺘﻔﺎده
20
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻋﺎﺑﺪﻳﻦ وﻛﻴﻠﻲ و ﻫﻤﻜﺎران
408
ﺷﺪ 21.ﺑﺮاي اﻧﺪازهﮔﻴﺮي ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ
ﺧﻠﻔﻲ ﻣﻐﺰ را ﺑﻪﻃﻮر ﻣﻌﻨﻲداري در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﮔﺮوه ﺳﺎﻟﻴﻦ ﻛﺎﻫﺶ داد
ﻣﻐﺰ 250 ،ﻣﻴﻜﺮوﻟﻴﺘﺮ از ﻣﺤﻠﻮل روﻳﻲ ﻧﻤﻮﻧﻪ اوﻟﻴﻪ را ﺑﺎ 1/5ﻣﻴﻠﻲﻟﻴﺘﺮ
) ،P<0/001ﻧﻤﻮدار .(3درﺻﺪ ﻣﺤﺘﻮاي آب ﻣﻐﺰ ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ
اﺳﻴﺪ ﻓﺴﻔﺮﻳﻚ %1و ﻧﻴﻢ ﻣﻴﻠﻲﻟﻴﺘﺮ ﻣﺤﻠﻮل آﺑﻲ ﺗﻴﻮﺑﺎرﺑﻴﺘﻮرﻳﻚ اﺳﻴﺪ 0/6
ﺑﻌﺪ از ﺟﺮاﺣﻲ در ﻧﻴﻢﻛﺮهﻫﺎي ﭼﭗ )ﻏﻴﺮ اﻳﺴﻜﻤﻴﻚ( در ﮔﺮوه ﻛﻨﺘﺮل
درﺻﺪ ﻣﺨﻠﻮط ﻛﺮده و ﺑﻪﻣﺪت 45دﻗﻴﻘﻪ در دﺳﺘﮕﺎه ﺑﻦ ﻣﺎري ﻗﺮار داد
ﻛﺎذب ،78/2±0/3ﮔﺮوه ﻛﻨﺘﺮل ﺳﺎﻟﻴﻦ 78/4±0/3و در ﮔﺮوه زﻋﻔﺮان
ﻣﻲﺷﺪ .ﭘﺲ از ﺧﻨﻚ ﺷﺪن دو ﻣﻴﻠﻲﻟﻴﺘﺮ ﻣﺤﻠﻮل n-butanolﺑﻪ ﻣﺤﻠﻮل
78/5±0/32ﺑﻮد ﻛﻪ اﺧﺘﻼف ﻣﻌﻨﻲداري وﺟﻮد ﻧﺪاﺷﺖ )،P>0/05
ﻓﻮق اﻓﺰوده ﺷﺪه و ﺑﻪﻣﺪت 10دﻗﻴﻘﻪ در 3000Gﺳﺎﻧﺘﺮﻳﻔﻴﻮژ ﮔﺮدﻳﺪ.
ﻧﻤﻮدار .(3اﻳﺠﺎد ﺳﻜﺘﻪ ﻣﻐﺰي ﻣﻮﺿﻌﻲ ﺑﻪﻃﻮر ﻣﻌﻨﻲداري ﺑﺎﻋﺚ اﻓﺰاﻳﺶ
ﻣﺤﻠﻮل روﻳﻲ ﻧﻤﻮﻧﻪ ﺑﻪ ﻳﻚ ﻟﻮﻟﻪ ﺗﺎزه ﻣﻨﺘﻘﻞ ﮔﺸﺘﻪ و ﺟﺬب ﻧﻮري آن در
درﺻﺪ ﻣﺤﺘﻮاي آب ﻣﻐﺰ در ﻧﻴﻢﻛﺮه اﻳﺴﻜﻤﻴﻚ ) (82/4±0/78و ﭼﻬﺎر
ﻃﻮل ﻣﻮج 535ﻧﺎﻧﻮﻣﺘﺮ اﻧﺪازهﮔﻴﺮي ﮔﺮدﻳﺪ و ﺑﺎ ﻣﻨﺤﻨﻲ اﺳﺘﺎﻧﺪارد ﻛﻪ از
درﺻﺪي ادم ﻣﻐﺰي ﺷﺪ ) ،P<0/001ﻧﻤﻮدار .(4ﺗﺠﻮﻳﺰ زﻋﻔﺮان ﺑﺎ دوز
ﻣﺤﻠﻮلﻫﺎي اﺳﺘﺎﻧﺪارد ﺗﻬﻴﻪ ﺷﺪه از -3 ،3 ،1 ،1ﺗﺘﺮاﻣﺘﻴﻞ ﭘﺮوﭘﺎن
100mg/kgدر ﺷﺮوع اﻳﺴﻜﻤﻲ ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻣﻌﻨﻲدار درﺻﺪ ﻣﺤﺘﻮاي
ﺑﻪدﺳﺖ آﻣﺪه ﺑﻮد ،ﺧﻮاﻧﺪه ﺷﺪ .ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ ﺑﺮ ﺣﺴﺐ
آب ﻣﻐﺰ ) (80/1±0/43ﺷﺪه و ادم ﻣﻐﺰي را ﺑﻪﻣﻴﺰان %60در ﻣﻘﺎﻳﺴﻪ
ﻧﺎﻧﻮﻣﻮل ﺑﺮ ﻣﻴﻠﻲﮔﺮم ﭘﺮوﺗﻴﻴﻦ ﺑﻴﺎن ﺷﺪ 21.ﻧﺘﺎﻳﺞ ﺑﻪﺻﻮرت
ﻣﻴﺎﻧﮕﻴﻦ±
ﺑﺎ ﮔﺮوه ﻛﻨﺘﺮل ﻳﺎ ﺳﺎﻟﻴﻦ ﻛﺎﻫﺶ داد ) ،P<0/001ﻧﻤﻮدار .(4
اﻧﺤﺮاف ﻣﻌﻴﺎر ) (MeanSDﺑﻴﺎن ﺷﺪه اﺳﺖ .آزﻣﻮن آﻣﺎري ﻧﺸﺎن داد
-3ﺗﺎﺛﻴﺮ زﻋﻔﺮان ﺑﺮ ﻏﻠﻈﺖ ﺑﺎﻓﺘﻲ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ در ﻛﻮرﺗﻜﺲ ﻣﻐﺰ:
ﺗﻮزﻳﻊ داده در ﻣﻮرد درﺻﺪ آب ﻣﻐﺰ و آﻧﺰﻳﻢﻫﺎي آﻧﺘﻲاﻛﺴﻴﺪانﻫﺎ ﻧﺮﻣﺎل
ﻏﻠﻈﺖ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ در ﻛﻮرﺗﻜﺲ ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ از
One Way
ﺟﺮاﺣﻲ در ﮔﺮوه ﻛﻨﺘﺮل ﻛﺎذب 2/2±0/38nmol/mg Proteinﺑﻮد،
و روش Dennett'sﺑﻪﻋﻨﻮان Post-hoc analysisﺑﺮاي آﻧﺎﻟﻴﺰ
اﻳﺠﺎد ﺳﻜﺘﻪ ﻣﻐﺰي ﻣﻮﺟﺐ اﻓﺰاﻳﺶ ﻏﻠﻈﺖ ﺑﺎﻓﺘﻲ ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ
آﻣﺎري اﺳﺘﻔﺎده ﮔﺮدﻳﺪ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ آزﻣﻮن آﻣﺎري ﻧﺸﺎن داد ﺗﻮزﻳﻊ
) (3/6±0/27nmol/mg Proteinﺑﻪﻣﻴﺰان ﻣﻌﻨﻲدار ﮔﺮدﻳﺪ ).(P≤0/001
داده در ﻣﻮرد ﺣﺠﻢ ﺿﺎﻳﻌﺎت ﻣﻐﺰي ﻧﺮﻣﺎل ﻧﺒﻮد ،ﺑﺮاي ﻣﻘﺎﻳﺴﻪ ﺑﻴﻦ دو
ﺗﺠﻮﻳﺰ زﻋﻔﺮان در ﺷﺮوع اﻳﺴﻜﻤﻲ ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻣﻌﻨﻲدار ﻏﻠﻈﺖ ﺑﺎﻓﺘﻲ
ﮔﺮوه از آزﻣﻮن Mann-Whitney U-testﺑﺮاي آﻧﺎﻟﻴﺰ آﻣﺎري اﺳﺘﻔﺎده
ﻣﺎﻟﻮن دي آﻟﺪﻳﻴﺪ ) (3/1±0/26nmol/mg Proteinﺷﺪ ).(P≤0/001
ﺑﻮد ،ﺑﻨﺎﺑﺮاﻳﻦ ﺑﺮاي ﻣﻘﺎﻳﺴﻪ ﺑﻴﻦ ﮔﺮوهﻫﺎ از آزﻣﻮن ﭘﺎرﻣﺘﺮﻳﻚ ANOVA
ﺷﺪ .در ﺻﻮرﺗﻲﻛﻪ
P<0/05
ﻣﻲﮔﺮدﻳﺪ .از ﻧﺮماﻓﺰار
ﺑﻮد اﺧﺘﻼف ﺑﻴﻦ ﮔﺮوه ﻣﻌﻨﻲدار ﺗﻠﻘﻲ
-4ﺗﺎﺛﻴﺮ زﻋﻔﺮان ﺑﺮ ﻓﻌﺎﻟﻴﺖ ﺑﺎﻓﺘﻲ آﻧﺰﻳﻢ ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز و
(SigmaStat 3.0, Jandel Scientific, Erkrath
ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ در ﻛﻮرﺗﻜﺲ ﻣﻐﺰ :ﻓﻌﺎﻟﻴﺖ ﺑﺎﻓﺘﻲ آﻧﺰﻳﻢ ﺳﻮﭘﺮ اﻛﺴﻴﺪ
) Germanyﺑﺮاي آﻧﺎﻟﻴﺰ ﻧﺘﺎﻳﺞ اﺳﺘﻔﺎده ﺷﺪ.
دﻳﺲﻣﻮﺗﺎز در ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ،ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ از ﺟﺮاﺣﻲ در ﮔﺮوه ﻛﻨﺘﺮل ﻛﺎذب 22±0/33U/mg Proteinﺑﻮد ،اﻳﺠﺎد ﺳﻜﺘﻪ ﻣﻐﺰي
ﻳﺎﻓﺘﻪﻫﺎ
ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻣﻌﻨﻲداري ﻓﻌﺎﻟﻴﺖ ﺑﺎﻓﺘﻲ آﻧﺰﻳﻢ ﺳﻮﭘﺮ اﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز
-1ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ :ﻣﺴﺪود ﻛﺮدن ﺷﺮﻳﺎن ﻣﻴﺎﻧﻲ ﻣﻐﺰ ﺑﺎﻋﺚ
) (15/3±0/28U/mg Proteinدر ﻛﻮرﺗﻜﺲ ﺷﺪ ) ،P≤0/001ﻧﻤﻮدار .(5
ﺷﺪه اﺳﺖ ﺗﺎ ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ ﺑﻪ ﻛﻤﺘﺮ از 15درﺻﺪ ﺳﻄﺢ ﭘﺎﻳﻪ در
در ﺣﺎﻟﻲﻛﻪ ﺗﺰرﻳﻖ زﻋﻔﺮان در ﺷﺮوع اﻳﺴﻜﻤﻲ ﺑﺎﻋﺚ اﻓﺰاﻳﺶ ﻣﻌﻨﻲدار
ﻫﺮ دو ﮔﺮوه ﺳﺎﻟﻴﻦ )ﻛﻨﺘﺮل اﻳﺴﻜﻤﻴﻚ( و زﻋﻔﺮان ﻛﺎﻫﺶ ﺑﻴﺎﺑﺪ .اﮔﺮﭼﻪ
ﻓﻌﺎﻟﻴﺖ
)Protein
ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ در ﻃﻮل 60دﻗﻴﻘﻪ اﻳﺴﻜﻤﻲ در ﮔﺮوه زﻋﻔﺮان
(16/2±0/37U/mgدر ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ﺷﺪ ) .(P<0/001ﻓﻌﺎﻟﻴﺖ ﺑﺎﻓﺘﻲ
ﻛﻤﺘﺮ از ﮔﺮوه ﺳﺎﻟﻴﻦ ﺑﻮده اﺳﺖ وﻟﻲ اﻳﻦ اﺧﺘﻼف ﺑﻴﻦ دو ﮔﺮوه
آﻧﺰﻳﻢ ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ در ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ
ﻣﻌﻨﻲدار ﻧﺒﻮد ) ،P>0/05ﻧﻤﻮدار .(1
از ﺟﺮاﺣﻲ در ﮔﺮوه ﻛﻨﺘﺮل ﻛﺎذب 0/32±0/02 U/mg Proteinﺑﻮد،
ﺑﺎﻓﺘﻲ
آﻧﺰﻳﻢ
ﺳﻮﭘﺮ
اﻛﺴﻴﺪ
دﻳﺲﻣﻮﺗﺎز
-2ﺗﺎﺛﻴﺮ زﻋﻔﺮان ﺑﺮ ﻣﻴﺰان آﺳﻴﺐ و ادم ﻣﻐﺰي :ﺗﺠﻮﻳﺰ زﻋﻔﺮان در
اﻳﺠﺎد ﺳﻜﺘﻪ ﻣﻐﺰي ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﻣﻌﻨﻲداري ﻓﻌﺎﻟﻴﺖ ﺑﺎﻓﺘﻲ آﻧﺰﻳﻢ
ﺷﺮوع ﺳﻜﺘﻪ ﻣﻐﺰي ﺑﺎﻋﺚ ﻛﺎﻫﺶ 77درﺻﺪي ﺣﺠﻢ آﺳﻴﺐ ﻣﻐﺰي
ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ ) (0/26±0/02U/mg Proteinدر ﻛﻮرﺗﻜﺲ ﺷﺪ
) 45±11ﻣﻴﻠﻲﻣﺘﺮ ﻣﻜﻌﺐ( در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﮔﺮوه ﻛﻨﺘﺮل اﻳﺴﻜﻤﻴﻚ ﻳﺎ
) ،P≤0/001ﻧﻤﻮدار .(6در ﺣﺎﻟﻲﻛﻪ ﺗﺰرﻳﻖ زﻋﻔﺮان در ﺷﺮوع اﻳﺴﻜﻤﻲ
ﺳﺎﻟﻴﻦ ) (201±25mm3ﺷﺪ ) ،P<0/001ﻧﻤﻮدار .(2ﻋﻼوه ﺑﺮ اﻳﻦ
ﺑﺎﻋﺚ اﻓﺰاﻳﺶ ﻣﻌﻨﻲدار ﻓﻌﺎﻟﻴﺖ ﺑﺎﻓﺘﻲ آﻧﺰﻳﻢ ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪ
زﻋﻔﺮان ﺳﻄﺢ آﺳﻴﺐ ﻣﻐﺰي را از ﺑﺮش دو ﺗﺎ ﭘﻨﺞ ﺳﻄﺢ ﻗﺪاﻣﻲ ﺑﻪﺳﻤﺖ
) (0/29±0/01U/mg Proteinدر ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ﺷﺪ ).(P<0/001
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
409
اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ زﻋﻔﺮان در آﺳﻴﺐﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ اﻳﺴﻜﻤﻲ ﻣﻐﺰي در ﻣﻮش
ﻧﻤﻮدار :1-ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ ﻣﻐﺰ ﻗﺒﻞ و در ﻃﻮل 60دﻗﻴﻘﻪ اﻧﺴﺪاد ﺷﺮﻳﺎن ﻣﻴﺎﻧﻲ ﻣﻐﺰ و 15دﻗﻴﻘﻪ ﺑﻌﺪ از ﺑﺮﻗﺮاري ﺟﺮﻳﺎن ﺧﻮن در ﮔﺮوه ﺳﺎﻟﻴﻦ )ﺷﺎﻫﺪ( و زﻋﻔﺮان
2
ﻧﻤﻮدار :3-ﺳﻄﺢ آﺳﻴﺐ ﻣﻐﺰي ) (mmدر ﻫﻔﺖ ﺑﺮش ﻣﻐﺰي از ﻗﺴﻤﺖ ﻗـﺪاﻣﻲ ﺑـﻪ ﺑﺨﺶ ﺧﻠﻔﻲ ﻣﻐﺰ در ﮔﺮوهﻫﺎي ﺳﺎﻟﻴﻦ )ﺷﺎﻫﺪ( و زﻋﻔﺮان ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ از اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ در ﻣﻮش ﺻﺤﺮاﻳﻲ
ﻧﻤﻮدار :2-ﺣﺠﻢ آﺳﻴﺐ ﻣﻐﺰي ) (mm3در ﮔﺮوهﻫـﺎي ﺳـﺎﻟﻴﻦ )ﺷـﺎﻫﺪ( و زﻋﻔـﺮان ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ از اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ در ﻣﻮش ﺻﺤﺮاﻳﻲ ﻧﻤﻮدار :4-درﺻﺪ ﻣﺤﺘﻮاي آب ﻣﻐﺰ در ﻧﻴﻢﻛﺮه اﻳﺴﻜﻤﻴﻚ )راﺳﺖ( و ﻧﻴﻢﻛـﺮه ﻏﻴـﺮ
ﺑﺤﺚ
اﻳﺴﻜﻤﻴﻚ )ﭼﭗ( در ﮔﺮوهﻫﺎي ﺷﻢ )ﻛﻨﺘﺮل ﻛﺎذب( و ﺳـﺎﻟﻴﻦ )ﺷـﺎﻫﺪ( و زﻋﻔـﺮان
ﻧﺘﺎﻳﺞ ﭘﮋوﻫﺶ ﺣﺎﺿﺮ ﻧﺸﺎن داد ،زﻋﻔﺮان آﺳﻴﺐ ﻧﺎﺷﻲ از اﻳﺴﻜﻤﻲ
ﺑﻴﺴﺖ و ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﻌﺪ از ﺟﺮاﺣﻲ ﻳﺎ اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ در ﻣﻮش
ﻣﻐﺰي ﻣﻮﺿﻌﻲ را ﺑﻪﻣﻴﺰان زﻳﺎدي در ﻣﻮش ﺻﺤﺮاﻳﻲ ﻛﺎﻫﺶ ﻣﻲدﻫﺪ. اﻳﻦ ﻳﺎﻓﺘﻪ ﺗﺎ ﺣﺪودي ﻣﺸﺎﺑﻪ ﻣﻄﺎﻟﻌﻪ Saleemاﺳﺖ ﻛﻪ ﻧﺸﺎن داد ﻣﺼﺮف 14
ﺧﻮراﻛﻲ زﻋﻔﺮان ﻫﻔﺖ روز ﻗﺒﻞ از اﻳﺠﺎد اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ
اﻳﻦ ﻳﺎﻓﺘﻪ ﻧﻴﺰ ﻣﻲﺗﻮاﻧﺪ ﺗﺎﻳﻴﺪي ﺑﺮ ﻧﺘﺎﻳﺞ ﺗﺤﻘﻴﻖ ﺣﺎﺿﺮ ﺑﺎﺷﺪ .ﺑﻪدﻧﺒﺎل
ﻣﻲﺗﻮاﻧﺪ از آﺳﻴﺐ اﻛﺴﻴﺪاﺗﻴﻮ و ﻣﺮگ ﻧﺮوﻧﻲ در ﻣﻮش ﺻﺤﺮاﻳﻲ
ﻛﺎﻫﺶ ﻳﺎ ﻗﻄﻊ ﺟﺮﻳﺎن ﺧﻮن ﻣﻮﺿﻌﻲ ﻣﻐﺰ ،ﺳﻠﻮلﻫﺎي ﻋﺼﺒﻲ در ﻣﺮﻛﺰ
ﭘﻴﺶﮔﻴﺮي ﻧﻤﺎﻳﺪ 11.ﻫﻤﻴﻦﻃﻮر ﻳﺎﻓﺘﻪ ﻣﺎ ﺗﺎ ﺣﺪودي ﺑﺎ ﻧﺘﺎﻳﺞ ﻣﻄﺎﻟﻌﺎت
ﻗﻄﻊ ﺟﺮﻳﺎن ﺳﻠﻮل ﻋﺼﺒﻲ در ﻫﻤﺎن دﻗﺎﻳﻖ اوﻟﻴﻪ ﺳﻜﺘﻪ ﻣﻐﺰي از ﺑﻴﻦ
دﻳﮕﺮان ﻫﻢﺧﻮاﻧﻲ دارد ،ﻛﻪ در آن ﻧﺸﺎن داده ﺷﺪ ،زﻋﻔﺮان اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ
رﻓﺘﻪ و آﺳﻴﺐﻫﺎي اوﻟﻴﻪ را اﻳﺠﺎد ﻣﻲﻛﻨﻨﺪ .وﻟﻲ ﺳﻠﻮلﻫﺎي ﻋﺼﺒﻲ ﻛﻪ
ﻧﺎﺷﻲ از
ﺣﺎﺷﻴﻪ ﻣﺮﻛﺰ ﻗﻄﻊ ﺟﺮﻳﺎن ﺧﻮن )ﻧﺎﺣﻴﻪ (Penumbraﻗﺮار دارﻧﺪ ،زﻧﺪهاﻧﺪ
اﻳﺴﻜﻤﻲ را در ﻣﻮش ﺻﺤﺮاﻳﻲ دارد Joukar .ﻧﺸﺎن داد ،ﻣﺼﺮف
وﻟﻲ ﻓﺎﻗﺪ ﻋﻤﻠﻜﺮد ﻃﺒﻴﻌﻲ ﻫﺴﺘﻨﺪ و ﺑﻪﺗﺪرﻳﺞ ﻣﻤﻜﻦ اﺳﺖ از ﺑﻴﻦ رﻓﺘﻪ و
12
در ﻣﻘﺎﺑﻞ آﺳﻴﺐ اﻛﺴﻴﺪاﺗﻴﻮ در ﻛﻠﻴﻪ
13
و ﻋﻀﻠﻪ اﺳﻜﻠﺘﻲ
22
ﺧﻮراﻛﻲ زﻋﻔﺮان از ﻃﺮﻳﻖ ﺗﻘﻮﻳﺖ ﺳﻴﺴﺘﻢ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ اﺛﺮ
آﺳﻴﺐ ﺛﺎﻧﻮﻳﻪ ﭘﺲ از ﺳﻜﺘﻪ ﻣﻐﺰي را ﺑﻪوﺟﻮد آورﻧﺪ.
ﭘﻴﺶﮔﻴﺮيﻛﻨﻨﺪﮔﻲ در ﻣﻘﺎﺑﻞ آﺳﻴﺐ ﻗﻠﺒﻲ اﻟﻘﺎ ﺷﺪه ﺑﺎ اﻳﺰوﭘﺮﺗﺮاﻧﻮل دارد،
ﻋﺼﺒﻲ ﻣﺴﺘﻘﺮ در ﻧﺎﺣﻴﻪ Penumbraﻗﺎﺑﻠﻴﺖ ﺑﺎزﻳﺎﺑﻲ ﺑﻪوﺳﻴﻠﻪ داروﻫﺎي
ﺳﻠﻮلﻫﺎي
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻋﺎﺑﺪﻳﻦ وﻛﻴﻠﻲ و ﻫﻤﻜﺎران
410
ﻧﺮوﭘﺮوﺗﻜﺘﻴﻮ ﺑﺮاي آنﻫﺎ ﻣﺘﺼﻮر اﺳﺖ 23.ﻛﻮرﺗﻜﺲ ﻣﻐﺰ ﺑﻪدﻟﻴﻞ وﺟﻮد
رادﻳﻜﺎلﻫﺎي آزاد و ﺷﺮوع ﻣﺮگ ﺑﺮﻧﺎﻣﻪرﻳﺰي ﺷﺪه ﺳﻠﻮﻟﻲ اﻓﺰاﻳﺶ
ﺟﺮﻳﺎن ﺧﻮن ﺟﺎﻧﺒﻲ زﻳﺎد ﺑﺨﺶ اﺻﻠﻲ Penumbraﺑﻪ ﺧﻮد اﺧﺘﺼﺎص
ﻣﻲﻳﺎﺑﺪ ،ﻟﺬا ﺑﺮﮔﺮداﻧﺪن و ﻳﺎ ﺣﻔﻆ ﻓﻌﺎﻟﻴﺖ ﺳﻄﺢ داﺧﻞ ﺳﻠﻮﻟﻲ اﻳﻦ
در ﻫﻤﻴﻦ راﺳﺘﺎ ،ﻧﺘﺎﻳﺞ دﻳﮕﺮ اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻧﺸﺎن داد ،اﺛﺮ
آﻧﺰﻳﻢﻫﺎ ﺑﻪوﺳﻴﻠﻪ ﺗﺤﺮﻳﻚ اﻓﺰاﻳﺶ ﺳﻨﺘﺰ آن ﻣﻤﻜﻦ اﺳﺖ ﺳﻠﻮلﻫﺎ را در
ﻣﺤﺎﻓﻈﺘﻲ زﻋﻔﺮان ﻋﻤﺪﺗﺎ را در ﺑﺮش دو ﺗﺎ ﭘﻨﺞ ﻣﻐﺰي ﻛﻪ ﺑﺨﺶ اﻋﻈﻢ
ﻣﻘﺎﺑﻞ آﺳﻴﺐ و ﻣﺮگ ﻣﺤﺎﻓﻈﺖ ﻧﻤﺎﻳﺪ .ﺷﻮاﻫﺪ ﭘﮋوﻫﺸﻲ ﻧﺸﺎن ﻣﻲدﻫﻨﺪ،
ﻛﻮرﺗﻜﺲ ﻣﻐﺰ و ﻧﺎﺣﻴﻪ Penumbraرا ﺗﺸﻜﻴﻞ ﻣﻲدﻫﺪ ،ﻣﺸﺎﻫﺪه ﺷﺪه
زﻋﻔﺮان و ﻣﻮاد ﻣﻮﺛﺮه آن ﺳﻴﺴﺘﻢ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ را ﺗﻘﻮﻳﺖ ﻧﻤﻮده و
23و22
ﻣﻲدﻫﺪ.
15و11
ﻧﺘﺎﻳﺞ ﭘﮋوﻫﺶ ﺣﺎﺿﺮ
اﺳﺖ .ﻫﻢﭼﻨﻴﻦ در اﻳﻦ ﺗﺤﻘﻴﻖ ﺑﺮاي اوﻟﻴﻦﺑﺎر ﻣﺎ ﻧﺸﺎن دادﻳﻢ ،زﻋﻔﺮان
ﺗﻮﻟﻴﺪ رادﻳﻜﺎلﻫﺎي آزاد را ﻛﺎﻫﺶ ﻣﻲدﻫﺪ.
ﻣﻲﺗﻮاﻧﺪ ادم ﻣﻐﺰي را ﻛﻪ ﻳﻜﻲ از ﻋﻠﺖ اﺻﻠﻲ اﻳﺠﺎد و ﮔﺴﺘﺮش آﺳﻴﺐ
ﻫﻢ ﻧﺸﺎن داد ،زﻋﻔﺮان در ﺑﺎﻓﺖ اﻳﺴﻜﻤﻴﻚ ﻛﻮرﺗﻜﺲ ﻣﻐﺰ
ﺛﺎﻧﻮﻳﻪ ﭘﺲ از ﺳﻜﺘﻪ ﻣﻐﺰي اﺳﺖ را ﺑﻪﻣﻴﺰان ﻗﺎﺑﻞ ﻣﻼﺣﻈﻪاي در ﻣﺪل
ﭘﺮاﻛﺴﻴﺪاﺳﻴﻮن ﭼﺮﺑﻲﻫﺎي ﻏﺸﺎي ﺳﻠﻮلﻫﺎي ﻋﺼﺒﻲ را ﻛﺎﻫﺶ داده و
ﺗﺠﺮﺑﻲ اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ -ﻣﻮﻗﺘﻲ ﻛﺎﻫﺶ دﻫﺪ .اﮔﺮﭼﻪ ﺗﺎﻛﻨﻮن
ﻫﻤﻴﻦﻃﻮر ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢ آﻧﺘﻲاﻛﺴﻴﺪانﻫﺎ از ﻗﺒﻴﻞ ﺳﻮﭘﺮاﻛﺴﻴﺪ
ﻣﻄﺎﻟﻌﻪ ﻣﺸﺎﺑﻪاي در اﻳﻦ زﻣﻴﻨﻪ اﻧﺠﺎم ﻧﺸﺪه اﺳﺖ وﻟﻲ ﺑﺮﺧﻲ ﺷﻮاﻫﺪ ﻏﻴﺮ
دﻳﺲﻣﻮﺗﺎز ،ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪاز را ﺗﻘﻮﻳﺖ ﻣﻲﻧﻤﺎﻳﺪ .ﺑﻨﺎﺑﺮاﻳﻦ ﺑﻪﻧﻈﺮ
ﻣﺴﺘﻘﻴﻢ ﻧﺸﺎن دادهاﻧﺪ ﻛﺮوﺳﻴﻦ از اﺟﺰاي ﻣﻮﺛﺮ زﻋﻔﺮان اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ در
ﻣﻲآﻳﺪ در ﻣﻄﺎﻟﻌﻪ ﺣﺎﺿﺮ زﻋﻔﺮان از ﻃﺮﻳﻖ ﻛﺎﻫﺶ ﺗﻮﻟﻴﺪ رادﻳﻜﺎلﻫﺎي
ﻣﻘﺎﺑﻞ ﺗﺨﺮﻳﺐ ﺳﺪ ﺧﻮﻧﻲ ﻣﻐﺰي ﺑﻌﺪ از اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﮔﻠﻮﺑﺎل در
آزاد و اﻓﺰاﻳﺶ ﺳﻄﺢ ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ ﻣﺮگ ﻧﺮوﻧﻲ و ادم
ﻛﺎﻫﺶ ﻧﻔﻮذﭘﺬﻳﺮي ﻋﺮوق ﻣﻐﺰي در ﻃﻮل
ﻣﻐﺰي را در ﻣﺪل ﺗﺠﺮﺑﻲ اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ ﻛﺎﻫﺶ داده ﺑﺎﺷﺪ.
16
ﻣﻮش ﺳﻮري دارد.
TNF-α
)ﻓﺎﻛﺘﻮر
اﻳﺴﻜﻤﻲ ﻣﻲﺗﻮاﻧﺪ ﺷﺎﻫﺪي ﺑﺮ ﻛﺎﻫﺶ ادم ﻣﻐﺰي ﺑﺎﺷﺪ ﻛﻪ ﺗﺎ ﺣﺪودي
ﻫﻤﻴﻦﻃﻮر ﭘﮋوﻫﺶﻫﺎي اﺧﻴﺮ ﻧﺸﺎن دادهاﻧﺪ،
ﻣﻲﺗﻮاﻧﺪ ﻧﺘﺎﻳﺞ ﻣﻄﺎﻟﻌﻪ ﺣﺎﺿﺮ را ﺗﺎﻳﻴﺪ ﻧﻤﺎﻳﺪ 17.ﭘﮋوﻫﺶﻫﺎي اﺧﻴﺮ ﻧﺸﺎن
ﻧﻜﺮوزدﻫﻨﺪه ﺗﻮﻣﻮري -آﻟﻔﺎ( ﺑﻪﻋﻨﻮان ﻳﻚ ﻓﺎﻛﺘﻮر ﭘﻴﺶاﻟﺘﻬﺎﺑﻲ ﻧﻘﺶ
دادهاﻧﺪ اﺳﺘﺮسﻫﺎي اﻛﺴﻴﺪاﺗﻴﻮ در ﭘﺎﺗﻮژﻧﺰ ﻣﺮﺣﻠﻪ ﺣﺎد ﺳﻜﺘﻪ ﻣﻐﺰي
ﻣﻬﻤﻲ در ﭘﺎﺗﻮﻓﻴﺰﻳﻮﻟﻮژي ادم و آﺳﻴﺐ ﻣﻐﺰي ﭘﺲ از ﺗﺮوﻣﺎ و ﺳﻜﺘﻪ 29و28و17
ﻧﻘﺶ ﻣﺤﻮري دارﻧﺪ22.و 16اﻳﺠﺎد اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ -ﻣﻮﻗﺘﻲ ﺑﺎﻋﺚ
ﻣﻐﺰي دارد.
اﻓﺰاﻳﺶ ﺗﻮﻟﻴﺪ رادﻳﻜﺎلﻫﺎي آزاد ،ﻧﻴﺘﺮﻳﻚ اﻛﺴﺎﻳﺪ و ﻛﺎﻫﺶ ﺳﻄﺢ
زﻋﻔﺮان ﺳﻨﺘﺰ
ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢﻫﺎي آﻧﺘﻲاﻛﺴﻴﺪاﻧﺖ ﻣﺜﻞ ﺳﻮﭘﺮاﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز،
ﺷﻮاﻫﺪي وﺟﻮد دارد ﻛﻪ ﻧﺸﺎن ﻣﻲدﻫﺪ ،ﻛﺮوﺳﻴﻦ از ﺗﺮﻛﻴﺒﺎت ﻣﻮﺛﺮ
اﮔﺮﭼﻪ ﻣﻄﺎﻟﻌﻪاي وﺟﻮد ﻧﺪارد ﻛﻪ ﻧﺸﺎن دﻫﺪ،
TNF-α
در ﻃﻮل اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻬﺎر ﻣﻲﻧﻤﺎﻳﺪ ،اﻣﺎ
ﮔﻠﻮﺗﺎﺗﻴﻮن و ﻛﺎﺗﺎﻻز ﻣﻲﺷﻮد 11.رادﻳﻜﺎلﻫﺎي آزاد ﺑﻪوﺳﻴﻠﻪ آﻧﺰﻳﻢﻫﺎي
زﻋﻔﺮان ﻣﻲﺗﻮاﻧﺪ در ﻣﺤﻴﻂ In vitroﻣﺮگ ﻧﺮوﻧﻲ ﻧﺎﺷﻲ از
آﻧﺘﻲاﻛﺴﻴﺪان داﺧﻞ ﺳﻠﻮﻟﻲ از ﻗﺒﻴﻞ آﻧﺰﻳﻢﻫﺎي ﺳﻮﭘﺮاﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز،
ﻣﻬﺎر ﻧﻤﺎﻳﺪ 30.ﺑﻨﺎﺑﺮاﻳﻦ ﻣﻤﻜﻦ اﺳﺖ ﺑﺨﺸﻲ از اﺛﺮات ﻣﻔﻴﺪ زﻋﻔﺮان از
TNF-α
را
ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪاز و ﻛﺎﺗﺎﻻزﻫﺎ ﺑﺮداﺷﺘﻪ و ﺣﺬف ﻣﻲﺷﻮﻧﺪ 24.ﻛﺎﻫﺶ
ﻃﺮﻳﻖ ﻣﻬﺎر ﺳﻨﺘﺰ
ﺳﻄﺢ ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢﻫﺎي آﻧﺘﻲاﻛﺴﻴﺪانﻫﺎ در ﻃﻮل اﻳﺴﻜﻤﻲ ﻣﻐﺰي و
روﺷﻦ ﺷﺪن اﻳﻦ ادﻋﺎ و ﮔﻤﺎن در ﺳﻄﺢ ﺳﻠﻮﻟﻲ و ﻣﺪلﻫﺎي ﺣﻴﻮاﻧﻲ
اﻓﺰاﻳﺶ ﺗﻮﻟﻴﺪ رادﻳﻜﺎلﻫﺎي آزاد و اﻛﺴﻴﺪانﻫﺎ ﻣﺴﻴﺮﻫﺎي ﺳﻴﮕﻨﺎﻟﻴﻨﮓ
ﺳﻜﺘﻪ ﻣﻐﺰي ﻧﻴﺎز اﺳﺖ .ﺑﻪﻃﻮر ﺧﻼﺻﻪ ﻧﺘﺎﻳﺞ اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻧﺸﺎن داد،
آﺳﻴﺐرﺳﺎن ﻣﺨﺘﻠﻔﻲ از ﺟﻤﻠﻪ ﻣﺴﻴﺮ ﻣﺮگ ﺑﺮﻧﺎﻣﻪرﻳﺰي ﺷﺪه ﺳﻠﻮﻟﻲ را
زﻋﻔﺮان اﺛﺮ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ ﻗﻮي دارد و ﻣﻲﺗﻮاﻧﺪ از ﻃﺮﻳﻖ ﻛﺎﻫﺶ ﺗﻮﻟﻴﺪ
ﻓﻌﺎل ﻛﺮده و ﺑﺎﻋﺚ اﻓﺰاﻳﺶ آﺳﻴﺐ و در ﻧﻬﺎﻳﺖ ﻣﺮگ ﺳﻠﻮﻟﻲ
رادﻳﻜﺎلﻫﺎي آزاد و ﺗﻘﻮﻳﺖ ﺳﻴﺴﺘﻢ آﻧﺘﻲاﻛﺴﻴﺪاﻧﺘﻲ ﺳﻠﻮﻟﻲ ﻣﺮگ ﻧﺮوﻧﻲ
ﭘﮋوﻫﺶ ﻗﺒﻠﻲ ﮔﺰارش ﻛﺮدهاﻧﺪ ،ﻣﻬﺎرﻛﻨﻨﺪه ﭘﺮاﻛﺴﻴﺪاﺳﻴﻮن
و ادم ﻣﻐﺰي را در ﻣﺪل ﺗﺠﺮﺑﻲ اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ ﻛﺎﻫﺶ دﻫﺪ.
ﭼﺮﺑﻲ ﻏﺸﺎ و ﻳﺎ از ﺑﻴﻦ ﺑﺮﻧﺪهﻫﺎي رادﻳﻜﺎل آزاد اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ در ﻣﻘﺎﺑﻞ
ﺳﭙﺎﺳﮕﺰاري :اﻳﻦ ﺗﺤﻘﻴﻖ ﺑﺎ ﺣﻤﺎﻳﺖ ﻣﺎﻟﻲ داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺳﻤﻨﺎن
ﻫﻤﻴﻦﻃﻮر ﺗﺤﺮﻳﻚ اﻓﺰاﻳﺶ ﺑﻴﺎن آﻧﺰﻳﻢ
)ﻃﺮح ﺗﺤﻘﻴﻘﺎﺗﻲ ﺷﻤﺎره (312اﻧﺠﺎم ﺷﺪ .اﻳﻦ ﻣﻘﺎﻟﻪ ﺑﺨﺸﻲ از ﭘﺎﻳﺎنﻧﺎﻣﻪ
ﺳﻮﭘﺮاﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز ﺑﺎﻋﺚ ﻣﻘﺎوﻣﺖ ﺑﻴﺸﺘﺮ در ﺑﺮاﺑﺮ اﻳﺴﻜﻤﻲ و
آﻗﺎي ﻣﺤﻤﺪ رﺿﺎ ﻋﻴﻨﻌﻠﻲ داﻧﺸﺠﻮي ﻛﺎرﺷﻨﺎﺳﻲ ارﺷﺪ ﻓﻴﺰﻳﻮﻟﻮژي اﺳﺖ.
ﺑﺮﻋﻜﺲ ﺣﺬف آن ﺑﺎﻋﺚ اﻓﺰاﻳﺶ ﺣﺠﻢ ﺳﻜﺘﻪ ﻣﻐﺰي در ﻣﻮش ﺳﻮري
ﻧﻮﻳﺴﻨﺪﮔﺎن ﻣﻘﺎﻟﻪ از ﻫﻤﻜﺎري و ﻣﺴﺎﻋﺪت آﻗﺎي دﻛﺘﺮ ﻋﺒﺎﺳﻌﻠﻲ وﻓﺎﻳﻲ
ﻛﺎﻫﺶ ﺳﻄﺢ ﻓﻌﺎﻟﻴﺖ آﻧﺰﻳﻢﻫﺎي ﺳﻮﭘﺮاﻛﺴﻴﺪ دﻳﺲﻣﻮﺗﺎز،
اﺳﺘﺎد ﺗﻤﺎم ﮔﺮوه ﻓﻴﺰﻳﻮﻟﻮژي و دﻛﺘﺮ ﻋﻠﻲ رﺷﻴﺪي ﭘﻮر رﻳﺎﺳﺖ ﻣﺤﺘﺮم
ﮔﻠﻮﺗﺎﺗﻴﻮن ﭘﺮاﻛﺴﻴﺪاز در ﻃﻮل اﻳﺴﻜﻤﻲ ﻣﻐﺰي ﻣﻮﺿﻌﻲ ،اﺣﺘﻤﺎﻻ
ﻣﺮﻛﺰ ﺗﺤﻘﻴﻘﺎت ﻓﻴﺰﻳﻮﻟﻮژي داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺳﻤﻨﺎن ﻗﺪرداﻧﻲ و
ﺣﺴﺎﺳﻴﺖ ﺳﻠﻮلﻫﺎي ﻋﺼﺒﻲ را ﺑﻪﻋﻮاﻣﻞ آﺳﻴﺐرﺳﺎن از ﻗﺒﻴﻞ
ﺗﺸﻜﺮ ﻣﻲﻧﻤﺎﻳﻨﺪ.
16و11
ﻣﻲﺷﻮد.
25و7و1
ﺳﻜﺘﻪ ﻣﻐﺰي دارﻧﺪ.
27و26
ﻣﻲﺷﻮد.
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
TNF-α
اﻋﻤﺎل ﺷﺪه ﺑﺎﺷﺪ .ﻣﻄﺎﻟﻌﺎت ﺑﻴﺸﺘﺮي ﺑﺮاي
411
اﻛﺴﻴﺪاﺗﻴﻮ اﻳﺴﻜﻤﻲ ﻣﻐﺰي در ﻣﻮش Vakili ﻫﺎي A. etآﺳﻴﺐ al. اﺛﺮ ﻣﺤﺎﻓﻈﺘﻲ زﻋﻔﺮان در
References 1. Chan PH. Reactive oxygen radicals in signaling and damage in the ischemic brain. J Cereb Blood Flow Metab 2001;21(1):2-14. 2. Tarawneh R, Galvin JE. Potential future neuroprotective therapies for neurodegenerative disorders and stroke. Clin Geriatr Med 2010;26(1):125-47. 3. Silver IA, Erecińska M. Extracellular glucose concentration in mammalian brain: continuous monitoring of changes during increased neuronal activity and upon limitation in oxygen supply in normo-, hypo-, and hyperglycemic animals. J Neurosci 1994;14(8):5068-76. 4. Wilson JX. Antioxidant defense of the brain: a role for astrocytes. Can J Physiol Pharmacol 1997;75(10-11):1149-63. 5. Chen H, Yoshioka H, Kim GS, Jung JE, Okami N, Sakata H, et al. Oxidative stress in ischemic brain damage: mechanisms of cell death and potential molecular targets for neuroprotection. Antioxid Redox Signal 2011;14(8):1505-17. 6. Fraser PA. The role of free radical generation in increasing cerebrovascular permeability. Free Radic Biol Med 2011;51(5):96777. 7. Heo JH, Han SW, Lee SK. Free radicals as triggers of brain edema formation after stroke. Free Radic Biol Med 2005;39(1):51-70. 8. Rıos JL, Recio MC, Giner RM, Manez S. An update review of saffron and its active constituents. Phytother Res 1996;10:189-93. 9. Kianbakht S. A systematic review on pharmacology of saffron and its active constituents. J Med Plants 2009;28(4):1-23. [Persian] 10. Schmidt M, Betti G, Hensel A. Saffron in phytotherapy: pharmacology and clinical uses. Wien Med Wochenschr 2007;157(13-14):315-9. 11. Saleem S, Ahmad M, Ahmad AS, Yousuf S, Ansari MA, Khan MB, Ishrat T, Islam F. Effect of Saffron (Crocus sativus) on neurobehavioral and neurochemical changes in cerebral ischemia in rats. J Med Food 2006;9(2):246-53. 12. Hosseinzadeh H, Sadeghnia HR, Ziaee T, Danaee A. Protective effect of aqueous saffron extract (Crocus sativus L.) and crocin, its active constituent, on renal ischemia-reperfusion-induced oxidative damage in rats. J Pharm Pharm Sci 2005;8(3):387-93. 13. Hosseinzadeh H, Modaghegh MH, Saffari Z. Crocus sativus L. (Saffron) extract and its active constituents (crocin and safranal) on ischemia-reperfusion in rat skeletal muscle. Evid Based Complement Alternat Med 2009;6(3):343-50. 14. Joukar S, Najafipour H, Khaksari M, Sepehri G, Shahrokhi N, Dabiri S, Gholamhoseinian A, Hasanzadeh S. The effect of saffron consumption on biochemical and histopathological heart indices of rats with myocardial infarction. Cardiovasc Toxicol 2010;10(1):6671. 15. Ochiai T, Shimeno H, Mishima K, Iwasaki K, Fujiwara M, Tanaka H, Shoyama Y, Toda A, Eyanagi R, Soeda S. Protective effects of carotenoids from saffron on neuronal injury in vitro and in vivo. Biochim Biophys Acta 2007;1770(4):578-84. 16. Zheng YQ, Liu JX, Wang JN, Xu L. Effects of crocin on reperfusion-induced oxidative/nitrative injury to cerebral
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
microvessels after global cerebral ischemia. Brain Res 2007;1138:86-94. 17. Vakili A, Mojarrad S, Akhavan MM, Rashidy-Pour A. Pentoxifylline attenuates TNF-α protein levels and brain edema following temporary focal cerebral ischemia in rats. Brain Res 2011;1377:119-25. 18. Vakili A, Zahedi khorasani M. Post-ischemic treatment of pentoxifylline reduces cortical not striatal infarct volume in transient model of focal cerebral ischemia in rat. Brain Res 2007;1144:186-91. 19. Vakili A, Kataoka H, Plesnila N. Role of arginine vasopressin V1 and V2 receptors for brain damage after transient focal cerebral ischemia. J Cereb Blood Flow Metab 2005;25(8):1012-9. 20. Bradford MM. A rapid and sensitive method for the quantitation of microgram quantities of protein utilizing the principle of proteindye binding. Anal Biochem 1976;72:248-54. 21. Mihara M, Uchiyama M. Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem 1978;86(1):271-8. 22. Doyle KP, Simon RP, Stenzel-Poore MP. Mechanisms of ischemic brain damage. Neuropharmacology 2008;55(3):310-8. 23. Segura T, Calleja S, Jordan J. Recommendations and treatment strategies for the management of acute ischemic stroke. Expert Opin Pharmacother 2008;9(7):1071-85. 24. Kakita T, Suzuki M, Takeuchi H, Unno M, Matsuno S. Significance of xanthine oxidase in the production of intracellular oxygen radicals in an in-vitro hypoxia-reoxygenation model. J Hepatobiliary Pancreat Surg 2002;9(2):249-55. 25. Kontos HA. Oxygen radicals in cerebral ischemia: the 2001 Willis lecture. Stroke 2001;32:2712-6. 26. Kim GW, Kondo T, Noshita N, Chan PH. Manganese superoxide dismutase deficiency exacerbates cerebral infarction after focal cerebral ischemia/reperfusion in mice: implications for the production and role of superoxide radicals. Stroke 2002;33(3):80915. 27. Kondo T, Reaume AG, Huang TT, Murakami K, Carlson E, Chen S, et al. Edema formation exacerbates neurological and histological outcomes after focal cerebral ischemia in CuZn-superoxide dismutase gene knockout mutant mice. Acta Neurochir Suppl 1997;70:62-4. 28. Hosomi N, Ban CR, Naya T, Takahashi T, Guo P, Song XY, et al. Tumor necrosis factor-alpha neutralization reduced cerebral edema through inhibition of matrix metalloproteinase production after transient focal cerebral ischemia. J Cereb Blood Flow Metab 2005;25(8):959-67. 29. Sriram K, O'Callaghan JP. Divergent roles for tumor necrosis factor-alpha in the brain. J Neuroimmune Pharmacol 2007;2(2):140-53. 30. Soeda S, Ochiai T, Paopong L, Tanaka H, Shoyama Y, Shimeno H. Crocin suppresses tumor necrosis factor-alpha-induced cell death of neuronally differentiated PC-12 cells. Life Sci 2001;69(24):2887-98.
Tehran University Medical Journal;ﻫﻤﻜﺎران Vol. 69, وNo. 7, October 2011: 405-412
102
The protective effects of Saffron against the oxidative damage in a transient model of focal cerebral ischemia in rats
Abedin Vakili Ph.D.1* Mohammad Reza Eianali M.Sc.1 Ahmad Reza Bandegi Ph.D.2 1- Department and Research Center of Physiology, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran. 2- Department of Biochemistry, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran.
Received: July 12, 2011 Accepted: July 25, 2011
Abstract
Background: Numerous studies have shown the protective effects of saffron against oxidative damage in a global model of cerebral ischemia, but its effects on brain edema and oxidative ischemic injury in focal ischemic stroke are not completely understood. Therefore, this study was designed to investigate the effects of saffron on brain edema, infarct volume, antioxidant enzyme activity (glutathione peroxidase and superoxide dismutase) and concentration of malondialdehyde (MDA) in ischemic brain tissue in an experimental model of stroke. Methods: Focal brain ischemia was established with the temporary occlusion of the middle cerebral artery for one hour in rats. Saffron (100 mg/kg) was given intraperitoneally at the onset of ischemia. 24 hours later, brain edema and infarct volume were evaluated and glutathione peroxidase and superoxide dismutase activities and MDA concentration were measured in the ischemic brain tissue using a specific kit.
Results: The results showed that saffron reduced infarct volume by 77% (P<0.001) and brain edema by 60% (P<0.001) compared with the control group in 24 hours following ischemia. Moreover, saffron significantly reduced the content of MDA (P<0.001) and increased the activity of superoxide dismutase (P<0.001) and glutathione peroxidase (P<0.001) in the cortex of the ischemic brain tissue.
Conclusion: Saffron has protective effects against oxidative ischemic damage and brain edema in a transient model of focal cerebral ischemia in rats. This protective effect is probably induced by increasing the capacity of antioxidant enzymes and decreasing the production of free radicals. Keywords: Brain edema, focal cerebral ischemia, oxidative damage, rat, saffron. *
Corresponding author: Km 5 Road Damghan, Faculty of Medicine, Dept. and Research Center of Physiology, Semnan, Iran. Tel: +98-231-3354161 E-mail: Abvakili@yahoo.com
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
ﺳﺮوﻳﻜﺲ413- ﻣﻬﺮ ﺑﺎ419 ،1390 اﻛﺴﻲ ﺗﻬﺮان، ﻋﻠﻮم ﺑﺎﭘﺰﺷﻜﻲ داﻧﺸﮕﺎه ﻣﺤﻠﻮلﺪه ﭘﺰﺷﻜﻲ، اﺛﺮ داﻧﺸﻜ ﻣﻘﺎﻳﺴﻪﻣﺠﻠﻪ ﻧﺎﻣﻨﺎﺳﺐ ﺷﻤﺎرهدر،7زﻧﺎن ، 69زاﻳﻤﺎن دورهاﻟﻘﺎي ﺗﻮﺳﻴﻦ در ﺧﻮراﻛﻲ ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﻣﻘﺎﻳﺴﻪ اﺛﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ در اﻟﻘﺎي زاﻳﻤﺎن در زﻧﺎن ﺑﺎ ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ
ﭼﻜﻴﺪه
1
ﺷﻴﺮﻳﻦ ﻧﻴﺮوﻣﻨﺶ
ﻣﻌﺼﻮﻣﻪ داداش ﻋﻠﻴﻬﺎ
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1390/03/11 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/04/06 :
*2
زﻣﻴﻨﻪ و ﻫﺪف :ﺳﺮوﻳﻜﺲ ﻣﻄﻠﻮب و اﻧﻘﺒﺎﺿﺎت رﺣﻤﻲ دو ﻋﺎﻣﻞ اﺳﺎﺳﻲ در زاﻳﻤﺎن ﻫﺴﺘﻨﺪ و ﺑﺮاي ﻣﻮﻓﻘﻴﺖ اﻟﻘﺎي زاﻳﻤﺎن ﺣﺎﻳﺰ اﻫﻤﻴﺖ ﻫﺴﺘﻨﺪ .روشﻫﺎي ﻣﺨﺘﻠﻔﻲ ﺑﺮاي اﻟﻘﺎي زاﻳﻤﺎن وﺟﻮد دارد ﻛﻪ ﻣﻲﺗﻮان ﺑﻪ ﻣﻴﺰوﭘﺮوﺳﺘﻮل و
2
ﻣﻴﻨﺎ اﻛﺮﻣﻲ
اﻛﺴﻲﺗﻮﺳﻴﻦ اﺷﺎره ﻛﺮد .ﻫﺪف اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻣﻘﺎﻳﺴﻪ ﻛﺎراﻳﻲ و اﻳﻤﻨﻲ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ ﺟﻬﺖ اﻟﻘﺎي -1ﮔﺮوه ﭘﺮي ﻧﺎﺗﺎل
زاﻳﻤﺎن در اﻓﺮاد ﺑﺎ ﻣﻌﺎﻳﻨﻪ ﻧﺎﻣﻨﺎﺳﺐ ﺳﺮوﻳﻜﺲ ﻣﻲﺑﺎﺷﺪ .روش ﺑﺮرﺳﻲ :اﻳﻦ ﭘﮋوﻫﺶ ﻳﻚ ﻛﺎرآزﻣﺎﻳﻲ ﺑﺎﻟﻴﻨﻲ دوﺳﻮﻛﻮر
-2ﮔﺮوه زﻧﺎن و زاﻳﻤﺎن
اﺳﺖ 140 .ﺧﺎﻧﻢ ﺑﺎردار 34-42ﻫﻔﺘﻪ ﻣﺮاﺟﻌﻪﻛﻨﻨﺪه ﺑﻪ ﺑﻴﻤﺎرﺳﺘﺎن زﻧﺎن در ﻃﻲ ﺳﺎلﻫﺎي 1388-89ﻛﻪ ﻛﺎﻧﺪﻳﺪاي ﺧﺘﻢ
ﺑﻴﻤﺎرﺳﺘﺎن زﻧﺎن )ﻣﻴﺮزاﻛﻮﭼﻚ ﺧﺎن( ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان.
ﺣﺎﻣﻠﮕﻲ ﺑﻮده و ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ داﺷﺘﻨﺪ ﺑﺎ اﺳﺘﻔﺎده از ﺟﺪول اﻋﺪاد ﺗﺼﺎدﻓﻲ ﺑﻪ دو ﮔﺮوه ﺗﻘﺴﻴﻢ ﺷﺪﻧﺪ .ﻳﻚ ﮔﺮوه ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﺎ دوز اوﻟﻴﻪ 20ﻣﻴﻜﺮوﮔﺮم در ﺳﺎﻋﺖ ﻫﻤﺮاه ﺑﺎ ﭘﻼﺳﺒﻮي ورﻳﺪي و ﻳﻚ ﮔﺮوه اﻛﺴﻲﺗﻮﺳﻴﻦ ﺑﺎ دوز اوﻟﻴﻪ ﺷﺶ ﻣﻴﻠﻲﻳﻮﻧﻴﺖ در دﻗﻴﻘﻪ ﻫﻤﺮاه ﺑﺎ ﭘﻼﺳﺒﻮ ﺧﻮراﻛﻲ درﻳﺎﻓﺖ ﻧﻤﻮدﻧﺪ و در ﻫﺮ دو ﮔﺮوه در ﺻﻮرت ﻧﺎﻣﻨﺎﺳﺐ ﺑﻮدن اﻧﻘﺒﺎﺿﺎت دوز دارو اﻓﺰوده ﺷﺪ .در اداﻣﻪ زﻣﺎن ﺑﺴﺘﺮي ﺗﺎ زاﻳﻤﺎن ،ﻧﻮع زاﻳﻤﺎن و ﻋﻮارض داروﻳﻲ در ﻫﺮ دو ﮔﺮوه ﺑﺮرﺳﻲ ﺷﺪﻧﺪ .ﻳﺎﻓﺘﻪﻫﺎ :در ﮔﺮوه ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﻓﺎﺻﻠﻪ زﻣﺎﻧﻲ درﻳﺎﻓﺖ اوﻟﻴﻦ دوز ﺗﺎ زاﻳﻤﺎن ﻃﺒﻴﻌﻲ 11/07±3/62ﺳﺎﻋﺖ و در ﮔﺮوه اﻛﺴﻲﺗﻮﺳﻴﻦ 14/87±3/11ﺳﺎﻋﺖ ﺑﻮد ﻛﻪ ﺑﻪﻣﻴﺰان ﻣﻌﻨﻲداري در ﮔﺮوه ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﻛﻢﺗﺮ ﺑﻮد ) .(P=0/001ﻧﻮع زاﻳﻤﺎن و ﻫﻢﭼﻨﻴﻦ ﻣﻴﺰان ﻓﺮاواﻧﻲ ﻋﻮارض داروﻳﻲ در دو ﮔﺮوه اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري ﻧﺪاﺷﺖ ) .(P>0/05ﻧﺘﻴﺠﻪﮔﻴﺮي :ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﻧﻪﺗﻨﻬﺎ داروﻳﻲ اﻳﻤﻦ و ﻛﺎرا در اﻟﻘﺎي
*
زاﻳﻤﺎن در اﻓﺮاد ﺑﺎ ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ ﻣﻲﺑﺎﺷﺪ ﺑﻠﻜﻪ ﻧﺴﺒﺖ ﺑﻪ اﻛﺴﻲﺗﻮﺳﻴﻦ ﻓﺎﺻﻠﻪ ﺑﻴﻦ ﺷﺮوع اﻳﻨﺪاﻛﺸﻦ ﺗﺎ زاﻳﻤﺎن ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﺗﻬﺮان ،ﺧﻴﺎﺑﺎن ﻛﺮﻳﻢﺧﺎن ،ﺑﻴﻤﺎرﺳﺘﺎن
زﻧﺎن )ﻣﻴﺮزاﻛﻮﭼﻚ ﺧﺎن( ،ﮔﺮوه زﻧﺎن زاﻳﻤﺎن
واژﻳﻨﺎل را ﻛﻮﺗﺎهﺗﺮ ﻣﻲﻛﻨﺪ.
ﺗﻠﻔﻦ021-88900002 : E-mail: dadashaliha@razi.tums.ac.ir
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :ﻣﻴﺰوﭘﺮوﺳﺘﻮل ،اﻛﺴﻲﺗﻮﺳﻴﻦ ،اﻟﻘﺎي زاﻳﻤﺎن ،ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ.
واژﻳﻨﺎل و ﺧﻮراﻛﻲ ﺟﻬﺖ آﻣﺎدهﺳﺎزي ﺳﺮوﻳﻜﺲ و ﺑﻬﺒﻮد اﻧﻘﺒﺎﺿﺎت
ﻣﻘﺪﻣﻪ
رﺣﻤﻲ اﺳﺘﻔﺎده ﻣﻲﺷﻮد .ﺗﻜﻨﻴﻚﻫﺎي ﻣﻜﺎﻧﻴﻜﻲ ﺷﺎﻣﻞ ﻛﺎﺗﺘﺮ ﺗﺮاﻧﺲ
اﻧﺪﻳﻜﺎﺳﻴﻮنﻫﺎي ﻣﺘﻌﺪدي ﺑﺮاي اﻟﻘﺎي زاﻳﻤﺎن ) (Laborوﺟﻮد دارد ﻛﻪ
ﺳﺮوﻳﻜﺎل ،اﻧﻔﻮزﻳﻮن ﺧﺎرج آﻣﻨﻴﻮﻧﻲ ﺳﺎﻟﻴﻦ ) ،(EASIﻣﺘﺴﻊﻛﻨﻨﺪهﻫﺎي
از آن ﺟﻤﻠﻪ ﻣﻲﺗﻮان ﺑﻪ ﺣﺎﻣﻠﮕﻲ ﭘﺴﺖﺗﺮم ،ﭘﺮهاﻛﻼﻣﭙﺴﻲ ،دﻳﺎﺑﺖ،
ﻫﻴﮕﺮوﺳﻜﻮﭘﻴﻚ ﻛﻪ ﺟﻬﺖ ﻣﺘﺴﻊ ﻛﺮدن ﺳﺮوﻳﻜﺲ ﻗﺒﻞ از اﻟﻘﺎي ﻟﻴﺒﺮ
اﻟﻴﮕﻮﻫﻴﺪراﻣﻨﻴﻮس ،ﭘﺎرﮔﻲ ﭘﺮدهﻫﺎ ،IUGR ،وﺿﻌﻴﺖ ﻏﻴﺮ اﻃﻤﻴﻨﺎنﺑﺨﺶ
اﺳﺘﻔﺎده ﻣﻲﺷﻮد .ﺳﺮوﻳﻜﺲ ﻣﻄﻠﻮب و اﻧﻘﺒﺎﺿﺎت رﺣﻤﻲ دو ﻋﺎﻣﻞ 2
ﺟﻨﻴﻦ و ﻏﻴﺮه اﺷﺎره ﻛﺮد 1.روشﻫﺎي ﻣﺨﺘﻠﻔﻲ ﻧﻴﺰ ﺑﺮاي اﻟﻘﺎي زاﻳﻤﺎن
اﺳﺎﺳﻲ در زاﻳﻤﺎن ﻫﺴﺘﻨﺪ .وﺿﻌﻴﺖ ﺳﺮوﻳﻜﺲ ﻳﺎ ﻣﻄﻠﻮب ﺑﻮدن آن
وﺟﻮد دارد ﻛﻪ ﺷﺎﻣﻞ ﺗﻜﻨﻴﻚﻫﺎي ﻓﺎرﻣﺎﻛﻮﻟﻮژﻳﻚ ﻣﺜﻞ اﻛﺴﻲﺗﻮﺳﻴﻦ ﻛﻪ
ﺑﺮاي ﻣﻮﻓﻘﻴﺖ اﻟﻘﺎي زاﻳﻤﺎن ﺣﺎﻳﺰ اﻫﻤﻴﺖ اﺳﺖ 3.ﺳﺮوﻳﻜﺲ ﻣﻄﻠﻮب ﻳﺎ
ﺑﻪﺻﻮرت داﺧﻞ ورﻳﺪي و ﺑﺎ اﺳﺘﻔﺎده از ﭘﻤﭗ اﻧﻔﻮزﻳﻮن ﺗﺠﻮﻳﺰ
ﻧﺮم ﻛﺮدن ﺳﺮوﻳﻜﺲ اﺷﺎره ﺑﻪ ﻛﻮﺗﺎﻫﻲ ،اﻓﺎﺳﻤﺎن و دﻳﻼﺗﺎﺳﻴﻮن
ﻛﻪ ﺑﻪﺻﻮرت
ﺳﺮوﻳﻜﺲ دارد ﻛﻪ ﺑﻪﻃﻮر ﻃﺒﻴﻌﻲ در ﭘﺎﻳﺎن ﺳﻪ ﻣﺎﻫﻪ ﺳﻮم ﻗﺒﻞ از زاﻳﻤﺎن
ﻣﻲﮔﺮدد ،ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦﻫﺎ ﻣﺎﻧﻨﺪ دﻳﻨﻮﭘﺮوﺳﺘﻮن
)(PGE2
واژﻳﻨﺎل اﺳﺘـﻔﺎده ﻣﻲﺷـﻮد و ﻣﻴـﺰوﭘﺮوﺳـﺘﻮل ) (PGE1ﻛـﻪ ﺑـﻪ دو روش
4
ﺧﻮد ﺑﻪﺧﻮد آﻏﺎز ﻣﻲﺷﻮد .ﻣﺘﺎﺳﻔﺎﻧﻪ در ﺑﺴﻴﺎري از ﻣﻮارد اﻧﺪﻳﻜﺎﺳﻴﻮن
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﺷﻴﺮﻳﻦ ﻧﻴﺮوﻣﻨﺶ و ﻫﻤﻜﺎران
414
اﻟﻘﺎ ،ﺳﺮوﻳﻜﺲ ﻓﺎﻗﺪ ﺣﺎﻟﺖ ﻣﻄﻠﻮب اﺳﺖ و ﻫﺮ ﭼﻪ ﺣﺎﻟﺖ ﻣﻄﻠﻮب ﻳﺎ
ﻣﺮاﺟﻌﻪﻛﻨﻨﺪه ﺑﻪ ﺑﻴﻤﺎرﺳﺘﺎن زﻧﺎن از ﺗﺎرﻳﺦ 1388/10/1ﻟﻐﺎﻳﺖ
اﻣﺘﻴﺎز ﺑﻴﺸﺎب ﻛﺎﻫﺶ ﻳﺎﺑﺪ ،ﻣﻴﺰان ﻣﻮﻓﻘﻴﺖ اﻟﻘﺎي زاﻳﻤﺎن ﺑﻪﻃﻮر
1389/10/1ﺑﻮدﻧﺪ ﭘﺮداﺧﺘﻴﻢ.
ﭘﻴﺶروﻧﺪه ﻛﺎﻫﺶ ﻣﻲﻳﺎﺑﺪ .ﺑﻪﻫﻤﻴﻦ دﻟﻴﻞ ﻧﻴﺎز ﺑﻪ ﻳﻚ روش ﻛﺎرا و اﻳﻤﻦ ﺟﻬﺖ آﻣﺎدهﺳﺎزي ﺳﺮوﻳﻜﺲ دارﻳﻢ .اﻛﺴﻲﺗﻮﺳﻴﻦ ﺑﺮ اﻧﻘﺒﺎﺿﺎت رﺣﻤﻲ
روش ﺑﺮرﺳﻲ
ﻣﻮﺛﺮ اﺳﺖ و ﺑﻪﺻﻮرت ﻣﺴﺘﻘﻴﻢ ﺗﺎﺛﻴﺮي ﺑﺮ اﻓﺎﺳﻤﺎن و دﻳﻼﺗﺎﺳﻴﻮن
ﭘﺲ از ﺗﺎﻳﻴﺪ ﻃﺮح ﺗﻮﺳﻂ ﻛﻤﻴﺘﻪ اﺧﻼق ﭘﺰﺷﻜﻲ ،ﺧﺎﻧﻢﻫﺎي ﺑﺎرداري
ﺳﺮوﻳﻜﺲ ﻧﺪارد .ﻛﺎرﺑﺮد آن ﻧﻴﺎز ﺑﻪ ﻛﺎﺗﺘﺮ ورﻳﺪي و ﭘﻤﭗ اﻧﻔﻮزﻳﻮن و
ﻛﻪ ﻛﺎﻧﺪﻳﺪ ﺧﺘﻢ ﺣﺎﻣﻠﮕﻲ و اﻟﻘﺎي زاﻳﻤﺎن ﺑﻮدﻧﺪ و از ﺗﺎرﻳﺦ 1388/10/1
ﭘﺎﻳﺶ ﻣﺴﺘﻘﻴﻢ دارد .ﻳﻜﻲ از روشﻫﺎي داروﻳﻲ ﺟﻬﺖ آﻣﺎدهﺳﺎزي
ﻟﻐﺎﻳﺖ 1389/10/1ﺑﻪ ﺑﻴﻤﺎرﺳﺘﺎن زﻧﺎن )ﻣﻴﺮزا ﻛﻮﭼﻚﺧﺎن( ﻣﺮاﺟﻌﻪ
ﺳﺮوﻳﻜﺲ اﺳﺘﻔﺎده از ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦﻫﺎ ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﺑﻴﺶ از ﻫﻤﻪ
ﻛﺮده و داراي ﻣﻌﻴﺎر ورود :ﺧﺎﻧﻢﻫﺎي ﺑﺎردار 18-40ﺳﺎﻟﻪ ﻛﻪ ﺑﻴﻦ
)دﻳﻨﻮﭘﺮوﺳﺘﻮن( ﺑﻪﺷﻜﻞ ژل ﻳﺎ ﺷﻴﺎف و ﻳﺎ
34-42ﻫﻔﺘﻪ ﺑﺎرداري ﺑﻮده .ﺣﺎﻣﻠﮕﻲ ﺗﻚﻗﻠﻮ ،ﭘﺮزاﻧﺘﺎﺳﻴﻮن ﺳﻔﺎﻟﻴﻚ،
ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦ ) E1ﻣﻴﺰوﭘﺮوﺳﺘﻮل( ﺑﻪﺷﻜﻞ ﻗﺮص از ﻃﺮﻳﻖ ﺧﻮراﻛﻲ ﻳﺎ
ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب ﻛﻢﺗﺮ از ﺷﺶ ،اﻧﻘﺒﺎﺿﺎت ﻧﺎﻛﺎﻓﻲ رﺣﻤﻲ )ﻛﻢﺗﺮ
واژﻳﻨﺎل ﺑﻪﻛﺎر ﻣﻲروﻧﺪ .ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦﻫﺎ ﺑﺎﻋﺚ اﻓﺰاﻳﺶ ﺗﺠﺰﻳﻪ
ﻳﺎ ﻣﺴﺎوي دو اﻧﻘﺒﺎض در 10دﻗﻴﻘﻪ( و Nst: normalو ﻧﺪاﺷﺘﻦ ﻣﻌﻴﺎر
ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦ
E2
ﻣﺎﺗﺮﻳﻜﺲ ﻛﻼژن ﺳﺮوﻳﻜﺲ ﻣﻲﺷﻮد و ﺑﺎ اﻳﻦ ﻛﺎر ﻣﻨﺠﺮ ﺑﻪ اﻓﺎﺳﻤﺎن و آﻣﺎدهﺷﺪن ﺳﺮوﻳﻜﺲ ﻣﻲﺷﻮد 5.ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦ
E2
ﺧﺮوج )ﭘﺎرﻳﺘﻲ≤،2
NST: abnormal
ﺳﺎﺑﻘﻪ اﺳﻜﺎر رﺣﻤﻲ ،ﺟﻔﺖ
)دﻳﻨﻮﭘﺮوﺳﺘﻮن(
ﺳﺮراﻫﻲ ،ﺧﻮنرﻳﺰي واژﻳﻨﺎل ﺑﻴﺶﺗﺮ از ﻧﻤﺎﻳﺶ ﺧﻮﻧﻲ زاﻳﻤﺎﻧﻲ ،ﺑﻴﻤﺎري
اوﻟﻴﻦ ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦ ﺷﻨﺎﺧﺘﻪ ﺷﺪه در اﻣﺮﻳﻜﺎ در دﻫﻪﻫﺎي ﮔﺬﺷﺘﻪ اﺳﺖ
ﻗﻠﺒﻲ .ﻛﻠﻴﻮي و ﻳﺎ ﻛﺒﺪي ﻣﺎدر ،اﻓﺰاﻳﺶ ﺣﺴﺎﺳﻴﺖ ﺑﻪ اﻛﺴﻲﺗﻮﺳﻴﻦ،
ﻛﻪ ﺑﺮاي آﻣﺎدهﺳﺎزي ﺳﺮوﻳﻜﺲ اﺳﺘﻔﺎده ﻣﻲﺷﻮد 6.دو اﺷﻜﺎل ﻋﻤﺪه دارد:
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﻳﺎ آﻧﺎﻟﻮگﻫﺎي ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦ( ﺑﻮدﻧﺪ ﭘﺲ از اﺧﺬ
ﻗﻴﻤﺖ آن ﮔﺮان اﺳﺖ و ﺑﺮاي ﻧﮕﻪداري از آن ﻧﻴﺎز ﺑﻪ ﻳﺨﭽﺎل دارﻳﻢ.
رﺿﺎﻳﺖﻧﺎﻣﻪ ﺗﻔﻬﻴﻤﻲ ﺟﻬﺖ ورود ﺑﻪ ﻃﺮح ،ﺑﻪﺻﻮرت ﺗﺼﺎدﻓﻲ ﺳﺎده ﺑﺎ
ﻣﻴﺰوﭘﺮوﺳﺘﻮل آﻧﺎﻟﻮگ PGE1و ﺳﻴﻨﺘﺘﻴﻚ اﺳﺖ ﻛﻪ ﻗﻴﻤﺖ آن ارزان اﺳﺖ
اﺳﺘﻔﺎده از ﺟﺪول اﻋﺪاد ﺗﺼﺎدﻓﻲ در ﻳﻜﻲ از دو ﮔﺮوه زﻳﺮ ) (A, Bﻗﺮار
و ﺑﺮاي ﻧﮕﻪداري آن ﻧﻴﺎز ﺑﻪ ﻳﺨﭽﺎل ﻧﻴﺴﺖ و در دﻣﺎي اﺗﺎق ﻗﺎﺑﻞ
ﮔﺮﻓﺘﻨﺪ و وارد ﻳﻚ ﻛﺎرآزﻣﺎﻳﻲ ﺑﺎﻟﻴﻨﻲ ﺗﺼﺎدﻓﻲ دوﺳﻮﻛﻮر ﺷﺪﻧﺪ .ﺗﻌﺪاد
ﻧﮕﻪداري اﺳﺖ و ﻋﻮارض ﺟﺎﻧﺒﻲ آن در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﭘﺮوﺳﺘﺎﮔﻼﻧﺪﻳﻦﻫﺎي
ﻧﻤﻮﻧﻪ 140ﻧﻔﺮ ﺑﻮد .در ﮔﺮوه 70 ،Aﻧﻔﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ
ﻃﺒﻴﻌﻲ ﻛﻢﺗﺮ اﺳﺖ و ﺑﺎﻋﺚ ﺷﺪه اﻳﻦ روش راﻫﻲ اﺳﺘﺎﻧﺪارد ﺟﻬﺖ
) (Highwycomble, Englandﺑﻪﻫﻤﺮاه ﭘﻼﺳﺒﻮي ورﻳﺪي و در ﮔﺮوه ،B
7
70ﻧﻔﺮ اﻛﺴﻲﺗﻮﺳﻴﻦ ورﻳﺪي )ﻛﺎﺳﭙﻴﻦ ،اﻳﺮان( ﺑﻪﻫﻤﺮاه ﭘﻼﺳﺒﻮي
آﻣﺎدهﺳﺎزي ﺳﺮوﻳﻜﺲ و اﻟﻘﺎي زاﻳﻤﺎن در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﻮد.
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﻫﻢ ﺑﺮ اﻧﻘﺒﺎﺿﺎت ﻣﻴﻮﻣﺘﺮ رﺣﻤﻲ ﻣﻮﺛﺮ اﺳﺖ و ﺑﺎ اﺛﺮ روي
ﺧﻮراﻛﻲ درﻳﺎﻓﺖ ﻛﺮدﻧﺪ .ﺑﻪ اﻳﻦ ﺻﻮرت ﻛﻪ در ﮔﺮوه
ﺳﺮوﻳﻜﺲ ﺑﺎﻋﺚ اﻓﺎﺳﻤﺎن و دﻳﻼﺗﺎﺳﻴﻮن آن ﻣﻲﺷﻮد و ﺑﺎ اﻳﻦ دو
200gﻣﻴﺰوﭘﺮوﺳﺘﻮل در 200mlآب ﺣﻞ ﺷﺪه و در ﭼﻬﺎر ﺳﺎﻋﺖ اول
ﻣﻜﺎﻧﻴﺴﻢ اﺣﺘﻤﺎل ﻣﻮﻓﻘﻴﺖ زاﻳﻤﺎن اﻓﺰاﻳﺶ ﻣﻲﻳﺎﺑﺪ .روشﻫﺎي ﻣﺨﺘﻠﻒ
ﻫﺮ ﺳﺎﻋﺖ 20ml= 20gو در ﺻﻮرت ﻧﺎﻛﺎﻓﻲ ﺑﻮدن اﻧﻘﺒﺎﺿﺎت ﭼﻬﺎر
ﺗﺠﻮﻳﺰ ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺷﺎﻣﻞ ﺧﻮراﻛﻲ ،زﻳﺮزﺑﺎﻧﻲ و واژﻳﻨﺎل اﺳﺖ.
ﺳﺎﻋﺖ دوم ﻫﺮ ﺳﺎﻋﺖ 40g= 40mlو در ﭼﻬﺎر ﺳﺎﻋﺖ ﺳﻮم ﻫﺮ
ﭘﻴﻚ ﺳﺮﻣﻲ ﻧﻮع ﺧﻮراﻛﻲ 34دﻗﻴﻘﻪ و ﻧﻴﻤﻪﻋﻤﺮ آن 20-40دﻗﻴﻘﻪ
ﺳﺎﻋﺖ 60g= 60mlاز ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل داده ﻣﻲﺷﺪ و در اﻳﻦ
اﺳﺖ وﻟﻲ ﭘﻴﻚ ﺳﺮﻣﻲ ﻣﻴﺰوﭘﺮوﺳﺘﻮل واژﻳﻨﺎل 60-80دﻗﻴﻘﻪ و ﺳﻄﺢ
ﻣﺪت اﻧﻘﺒﺎﺿﺎت رﺣﻤﻲ ﭼﻚ ﻣﻲﺷﺪ .در ﺻﻮرﺗﻲﻛﻪ اﻧﻘﺒﺎﺿﺎت ﻣﻨﺎﺳﺐ
ﺧﻮﻧﻲ آن ﺗﺎ ﭼﻬﺎر ﺳﺎﻋﺖ ﺑﺎﻗﻲ ﻣﻲﻣﺎﻧﺪ 8.اﺳﺘﻔﺎده از ﺷﻜﻞ ﺧﻮراﻛﻲ
)ﻓﻮاﺻﻞ اﻧﻘﺒﺎﺿﺎت 2-3دﻗﻴﻘﻪ و ﻫﺮ اﻧﻘﺒﺎض 60-90ﺛﺎﻧﻴﻪ ﻃﻮل
آﺳﺎنﺗﺮ ،ﻧﻴﻤﻪﻋﻤﺮ آن ﻛﻮﺗﺎهﺗﺮ و ﺷﺎﻧﺲ ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ آن ﻛﻢﺗﺮ
ﻣﻲﻛﺸﻴﺪ و ﻓﺸﺎر داﺧﻞ رﺣﻤﻲ 50-60ﻣﻴﻠﻲﻣﺘﺮ ﺟﻴﻮه( ﺑﻮد دوز ﺑﻌﺪي
اﺳﺖ 9.ﻫﻢاﻛﻨﻮن در ﺑﻴﻤﺎرﺳﺘﺎن زﻧﺎن )ﻣﻴﺮزاﻛﻮﭼﻚﺧﺎن( از اﻛﺴﻲﺗﻮﺳﻴﻦ
داده ﻧﻤﻲﺷﺪ .اﮔﺮ ﻣﺠﺪدا اﻧﻘﺒﺎﺿﺎت ﻧﺎﻛﺎﻓﻲ ﻣﻲﺷﺪ از 10gدر ﺳﺎﻋﺖ
ﺟﻬﺖ اﻟﻘﺎي زاﻳﻤﺎن اﺳﺘﻔﺎده ﻣﻲﺷﻮد .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻫﻤﻴﺖ ﻣﻮﺿﻮع و ﻧﻴﺰ
ﺷﺮوع و ﺑﻪ 20gو ﺣﺘﻲ ﺑﻪ 40gدر ﺳﺎﻋﺖ دوز را اﻓﺰاﻳﺶ داده ﺗﺎ
A
ﻳﻚ ﻗﺮص
ﻋﺪم وﺟﻮد ﻣﻄﺎﻟﻌﻪ ﻣﺸﺎﺑﻬﻲ در اﻳﺮان ،در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺑﻪﻣﻘﺎﻳﺴﻪ اﺛﺮ
زﻣﺎﻧﻲﻛﻪ اﻧﻘﺒﺎﺿﺎت ﻣﻨﺎﺳﺐ اﻳﺠﺎد ﮔﺮدد .در ﮔﺮوه
ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ و اﻛﺴﻲﺗﻮﺳﻴﻦ در اﻟﻘﺎي زاﻳﻤﺎن در
اﻛﺴﻲﺗﻮﺳﻴﻦ ورﻳﺪي اﺳﺘﻔﺎده ﺷﺪ ﻛﻪ 10واﺣﺪ در ﻳﻚ ﻟﻴﺘﺮ ﺳﺮم رﻳﻨﮕﺮ
ﺧﺎﻧﻢﻫﺎي ﺑﺎردار ﺑﺎ ﺳﻦ ﺣﺎﻣﻠﮕﻲ 34-42ﻛﻪ ﻛﺎﻧﺪﻳﺪ ﺧﺘﻢ ﺣﺎﻣﻠﮕﻲ و
رﻳﺨﺘﻪ و از 6mu/minﺷﺮوع و در ﻓﻮاﺻﻞ 20دﻗﻴﻘﻪ ،ﺷﺶ ﻣﻴﻠﻲﻳﻮﻧﻴﺖ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
B
از ﻣﺤﻠﻮل
415
ﻣﻘﺎﻳﺴﻪ اﺛﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ در اﻟﻘﺎي زاﻳﻤﺎن در زﻧﺎن ﺑﺎ ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ
اﻓﺰوده ﻣﻲﺷﺪ ﺗﺎ اﻧﻘﺒﺎﺿﺎت ﻛﺎﻓﻲ اﻳﺠﺎد ﺷﻮد و در ﺻﻮرت اﻳﺠﺎد ﺗﺎﻛﻲ
ﺟﻤﻊآوري اﻃﻼﻋﺎت ﻣﻮرد ﻧﻴﺎز ،اﻗﺪام ﺑﻪ ﺗﺠﺰﻳﻪ و ﺗﺤﻠﻴﻞ دادهﻫﺎي SPSS
ﺳﻴﺴﺘﻮل ﻳﺎ ﻫﻴﭙﺮﺗﻮﻧﻮس ﺗﺠﻮﻳﺰ اﻛﺴﻲﺗﻮﺳﻴﻦ ﻣﺘﻮﻗﻒ ﻣﻲﺷﺪ .در
ﺣﺎﺻﻠﻪ ﺷﺪ ﻛﻪ در اﻳﻦ زﻣﻴﻨﻪ از ﻧﺮماﻓﺰار آﻣﺎري
ﺻﻮرت اﻧﻘﺒﺎﺿﺎت ﻧﺎﻛﺎﻓﻲ رﺣﻤﻲ ﻣﺠﺪدا از دوز ﻛﻢ ﺷﺮوع و در
اﺳﺘﻔﺎده ﺷﺪ .ﺑﺮاي ﻣﻘﺎﻳﺴﻪ داده ﻛﻤﻲ در دو ﮔﺮوه ﻏﻴﺮواﺑﺴﺘﻪ از آزﻣﻮن
ﺻﻮرت ﻧﻴﺎز در ﻓﻮاﺻﻞ 20دﻗﻴﻘﻪاي دوز آن را اﻓﺰاﻳﺶ ﻣﻲدادﻳﻢ.
Independent sample t-testاﺳﺘﻔﺎده ﺷﺪ و ﺑﺮاي ﻣﻘﺎﻳﺴﻪ دادهﻫﺎي
وﻳﺮاﺳﺖ 17
2
ﺑﻴﻤﺎران در ﺗﻤﺎم ﻣﺪت ﺗﺤﺖ ﻣﺎﻧﻴﺘﻮرﻳﻨﮓ ﺿﺮﺑﺎن ﻗﻠﺐ ﺟﻨﻴﻦ ﺑﻮدﻧﺪ.
ﻛﻴﻔﻲ از آزﻣﻮن ﺑﻪﺗﻨﺎﺳﺐ اﺳﺘﻔﺎده ﺷﺪ .ﺳﻄﺢ ﻣﻌﻨﻲداري ﺑﺮاي ﺗﻔﺴﻴﺮ
ﻋﻼﻳﻢ ﺣﻴﺎﺗﻲ و ﮔﻮارﺷﻲ ﻣﺎ در ﻧﻴﺰ ﻫﺮ ﻳﻚ ﺳﺎﻋﺖ ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار
ﻧﺘﺎﻳﺞ 0/05ﻟﺤﺎظ ﮔﺮدﻳﺪ.
ﻣﻲﮔﺮﻓﺖ .ﻋﻮارض ﺟﺎﻧﺒﻲ دارو ﺷﺎﻣﻞ ﺗﺎﻛﻲ ﺳﻴﺴﺘﻮل )ﺷﺶ اﻧﻘﺒﺎض در 10دﻗﻴﻘﻪ ﻛﻪ ﺑﺮاي ﺣﺪاﻗﻞ 20دﻗﻴﻘﻪ ﻃﻮل ﺑﻜﺸﺪ( ،ﻫﻴﭙﺮﺗﻮﻧﻮس )ﺑﻪ ﻳﻚ
ﻳﺎﻓﺘﻪﻫﺎ
اﻧﻘﺒﺎض ﻛﻪ ﺑﻪﺗﻨﻬﺎﻳﻲ ﺑﺮاي ﺑﻴﺶﺗﺮ از دو دﻗﻴﻘﻪ ﻃﻮل ﺑﻜﺸﺪ( و
140ﺑﻴﻤﺎر ﻣﻮرد ﺑﺮرﺳﻲ ﻧﻬﺎﻳﻲ ﻗﺮار ﮔﺮﻓﺘﻨﺪ .ﻫﻴﭻ ﺑﻴﻤﺎري از ﻣﻄﺎﻟﻌﻪ
NST
ﺧﺎرج ﻧﺸﺪ و در ﻫﺮ دو ﮔﺮوه ﺗﺎ زﻣﺎن زاﻳﻤﺎن در ﺻﻮرت ﻧﻴﺎز ﺑﻪ
ﻏﻴﺮﻃﺒﻴﻌﻲ ﻣﺜﻞ اﻓﺖ دﻳﺮرس ،اﻓﺖ ﻣﺘﻐﻴﺮ ﺷﺪﻳﺪ ،اﻓﺖ ﻃﻮﻻﻧﻲﻣﺪت و ﻳﺎ
اﻳﻨﺪاﻛﺸﻦ ،ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﻳﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ اداﻣﻪ داده ﺷﺪ و در ﻫﻴﭻﻛﺪام
ﺗﺎﻛﻴﻜﺎردي ﻣﻨﺠﺮ ﺷﻮد ﮔﻔﺘﻪ ﻣﻲﺷﻮد ﻛﻪ اﺣﺘﻴﺎج ﺑﻪ ﻳﻚ ﻣﺪاﺧﻠﻪ ﺗﻮﻛﻮﻟﻴﺰ
ﺑﻪﻋﻠﺖ ﻋﻮارض داروﻳﻲ ﻣﺠﺒﻮر ﺑﻪ ﻗﻄﻊ دارو ﻧﺸﺪﻳﻢ .ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ،
ﻳﺎ زاﻳﻤﺎن داﺷﺘﻪ ﺑﺎﺷﻨﺪ[ و ﻋﻮارض ﮔﻮارﺷﻲ ﺷﺎﻣﻞ ﺗﻬﻮع ،اﺳﺘﻔﺮاغ،
ﮔﺮاوﻳﺪ ،ﭘﺎرﻳﺘﻲ و ﺳﻦ ﺑﺎرداري در دو ﮔﺮوه ﻫﻤﺴﺎن ﺑﻮد ).(P>0/05
اﺳﻬﺎل ،ﺗﺐ و ﺳﺮدرد ﻧﻴﺰ در دو ﮔﺮوه ﺑﺮرﺳﻲ ﺷﺪ .ﻣﺘﻮﺳﻂ ﻓﺎﺻﻠﻪ
ﻣﻴﺎﻧﮕﻴﻦ ﺑﻴﺸﺎب اﺳﻜﻮر ﺳﺮوﻳﻜﺲ در ﺣﻴﻦ ﺑﺴﺘﺮي در دو ﮔﺮوه ﻫﻤﺴﺎن
زﻣﺎﻧﻲ زاﻳﻤﺎن واژﻳﻨﺎل از ﺷﺮوع اﻟﻘﺎ ،ﻣﻴﺰان ﺳﺰارﻳﻦ ،ﻣﻴﺰان رﺿﺎﻳﺖﻣﻨﺪي
ﺑﻮد )) (P>0/05ﺟﺪول .(1ﻧﻮع زاﻳﻤﺎن )ﻃﺒﻴﻌﻲ و ﺳﺰارﻳﻦ( ،ﻋﻮارض
ﺑﻴﻤﺎران و آﭘﮕﺎر ﻧﻮزادان در ﻫﺮ دو ﮔﺮوه ﺑﺮرﺳﻲ و ﻣﻘﺎﻳﺴﻪ ﺷﺪ .ﭘﺲ از
داروﻳـﻲ )ﺳﺮدرد ،ﺗﻬﻮع ،اﺳﺘﻔﺮاغ ،اﺳﻬﺎل ،ﺧﻮنرﻳﺰي ،ﺗﺎﻛﻲ ﺳﻴﺴﺘﻮل و
ﺟﺪول :1-ﺗﻮزﻳﻊ ﻓﺮاواﻧﻲ ﻣﺘﻐﻴﺮﻫﺎي دﻣﻮﮔﺮاﻓﻴﻚ در دو ﮔﺮوه ﻣﻮرد ﻣﻄﺎﻟﻌﻪ
ﺟﺪول :2-ﺗﻮزﻳﻊ ﻓﺮاواﻧﻲ ﻋﻮارض داروﻳﻲ در دو ﮔﺮوه ﻣﻮرد ﻣﻄﺎﻟﻌﻪ
ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ ]ﺗﺎﻛﻲ ﺳﻴﺴﺘﻮل ﻳﺎ ﻫﻴﭙﺮﺗﻮﻧﻮس ﻛﻪ ﻣﻨﺠﺮ ﺑﻪ
ﻣﺘﻐﻴﺮ و ﮔﺮوه ﻣﺮﺑﻮﻃﻪ
ﻣﻴﺎﻧﮕﻴﻦ
اﻧﺤﺮافﻣﻌﻴﺎر
*P
ﻣﻴﺎﻧﮕﻴﻦ
اﻧﺤﺮافﻣﻌﻴﺎر
ﻣﻴﺰوﭘﺮوﺳﺘﻮل
11/07
3/62
اﻛﺴﻲﺗﻮﺳﻴﻦ
14/87
3/11
ﻣﺘﻐﻴﺮ و ﮔﺮوه ﻣﺮﺑﻮﻃﻪ
P
ﻓﺎﺻﻠﻪ اﻟﻘﺎ ﺗﺎ زاﻳﻤﺎن )ﺳﺎﻋﺖ(
ﺳﻦ )ﺳﺎل( ﻣﻴﺰوﭘﺮوﺳﺘﻮل
26/27
3/59
اﻛﺴﻲﺗﻮﺳﻴﻦ
27/00
3/9
0/025
ﻧﻮع زاﻳﻤﺎن
ﮔﺮاوﻳﺪ )ﺗﻌﺪاد ﺣﺎﻣﻠﮕﻲ( ﻣﻴﺰوﭘﺮوﺳﺘﻮل
1/34
0/50
اﻛﺴﻲﺗﻮﺳﻴﻦ
1/44
0/62
0/3
ﭘﺎرﻳﺘﻲ )ﺗﻌﺪاد زاﻳﻤﺎن( ﻣﻴﺰوﭘﺮوﺳﺘﻮل
0/21
0/41
اﻛﺴﻲﺗﻮﺳﻴﻦ
0/25
0/44
0/69
ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﻃﺒﻴﻌﻲ
%84/28
اﻛﺴﻲﺗﻮﺳﻴﻦ
ﻃﺒﻴﻌﻲ
%74/28
ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﺗﻬﻮع -اﺳﺘﻔﺮاغ
%21/42
اﻛﺴﻲﺗﻮﺳﻴﻦ
ﺗﻬﻮع -اﺳﺘﻔﺮاغ
%15/71
ﻣﻴﺰوﭘﺮوﺳﺘﻮل
38/94
اﻛﺴﻲﺗﻮﺳﻴﻦ
38/48
1/7
1/07
ﺑﻴﺸﺎب اﺳﻜﻮر )اﺑﺘﺪاي ﺑﺴﺘﺮي(
**0/55
ﺗﺎﻛﻲ ﺳﻴﺴﺘﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﺳﻦ ﺑﺎرداري )ﻫﻔﺘﻪ(
**0/107
ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﺎرﺿﻪ
اﻛﺴﻲﺗﻮﺳﻴﻦ
2/62
*0/001
ﺻﻔﺮ
--
ﺻﻔﺮ
--
--
ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﺻﻔﺮ
--
اﻛﺴﻲﺗﻮﺳﻴﻦ
ﺻﻔﺮ
--
--
رﺿﺎﻳﺖﻣﻨﺪي
ﻣﻴﺰوﭘﺮوﺳﺘﻮل
3/45
1/25
اﻛﺴﻲﺗﻮﺳﻴﻦ
3/32
1/16
* آزﻣﻮن آﻣﺎري ﻣﻮرد اﺳﺘﻔﺎده Student’s t-testو P<0/05ﻣﻌﻨﻲدار ﻣﻲﺑﺎﺷﺪ
0/34
ﻣﻴﺰوﭘﺮوﺳﺘﻮل
88/57
--
اﻛﺴﻲﺗﻮﺳﻴﻦ
78/57
--
**0/17
* آزﻣﻮن P<0/05 ،Student’s t-testﻣﻌﻨﻲدار ﻣﻲﺑﺎﺷﺪ ** آزﻣﻮن 2و P<0/05ﻣﻌﻨﻲدار ﻣﻲﺑﺎﺷﺪ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
416
ﺷﻴﺮﻳﻦ ﻧﻴﺮوﻣﻨﺶ و ﻫﻤﻜﺎران
ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ( و ﻣﻴﺰان رﺿﺎﻳﺖﻣﻨﺪي ﺑﻴﻤﺎران از ﻧﺤﻮه اﻟﻘﺎ در ﺑﻴﻦ دو
ﻣﻴﺰوﭘﺮوﺳﺘﻮل واژﻳﻨﺎل در 106ﺧﺎﻧﻢ ﺑﺎردار 34-42ﻫﻔﺘﻪ ﺑﺎرداري
ﮔﺮوه ﺗﻔﺎوت آﻣﺎري ﻣﻌﻨﻲداري ﻧﺪاﺷﺖ ) .(P>0/05ﺷﺎﻳﻊﺗـﺮﻳﻦ ﻋﺎرﺿـﻪ
ﻛﺎﻧﺪﻳﺪ اﻟﻘﺎي زاﻳﻤﺎن ﺑﺎ ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب ﻛﻢﺗﺮ از ﺷﺶ ﻣﻘﺎﻳﺴﻪ
داروﻳﻲ در دو ﮔﺮوه ﺗﻬﻮع اﺳﺘﻔﺮاغ ﺑﻮد .در دو ﮔﺮوه ﺗـﺎﻛﻲ ﺳﻴـﺴﺘﻮل و
ﺷﺪه ﺑﻪاﻳﻦ ﺻﻮرت ﻛﻪ در ﻧﻮع ﺧﻮراﻛﻲ ﻳﻚ ﻗﺮص 200ﻣﻴﻜﺮوﮔﺮﻣﻲ
ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ دﻳﺪه ﻧﺸﺪ .ﻣﻴﺎﻧﮕﻴﻦ ﻣﺪت زﻣﺎن اﻟﻘﺎ ﺗﺎ زاﻳﻤﺎن در ﮔﺮوه
در 200mlآب ﺣﻞ ﺷﺪه و در ﭼﻬﺎر ﺳﺎﻋﺖ اول ﻫﺮ ﺳﺎﻋﺖ 20mlو
ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﻧﺴﺒﺖ ﺑﻪ ﮔﺮوه اﻛﺴﻲﺗﻮﺳـﻴﻦ ﺑـﻪﻣﻴـﺰان
در ﭼﻬﺎر ﺳﺎﻋﺖ دوم ﻫﺮ ﺳﺎﻋﺖ 40mlو در ﭼﻬﺎر ﺳﺎﻋﺖ ﺳﻮم ﻫﺮ
ﻣﻌﻨﻲداري ﻛﻢ ﺗـﺮ ﺑـﻮد ) 11/07±3/62در ﺑﺮاﺑـﺮ 14/87±3/11ﺳـﺎﻋﺖ
ﺳﺎﻋﺖ 60mlداده ﻣﻲﺷﺪ ﺗﺎ ﻫﺮ زﻣﺎن ﻛﻪ اﻧﻘﺒﺎﺿﺎت ﻣﻨﺎﺳﺐ ﭘﻴﺪا ﻛﻨﺪ
.(P=0/001ﻣﻴﺎﻧﮕﻴﻦ آﭘﮕﺎر دﻗﻴﻘﻪ ﭘﻨﺠﻢ ﻧﻮزادان ﺑـﻴﻦ دو ﮔـﺮوه ﻣﺤﻠـﻮل
دوز ﺑﻌﺪي داده ﻧﻤﻲﺷﺪ و در ﮔﺮوه دﻳﮕﺮ 25ﻣﻴﻜﺮوﮔﺮم ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ و اﻛﺴﻲﺗﻮﺳﻴﻦ )ﺑﻪﺗﺮﺗﻴﺐ 9/45±0/82در ﺑﺮاﺑـﺮ
واژﻳﻨﺎل ﻫﺮ ﭼﻬﺎر ﺳﺎﻋﺖ ﮔﺬاﺷﺘﻪ ﺷﺪ .ﻧﺘﻴﺠﻪ اﻳﻦ ﻣﻄﺎﻟﻌﻪ زاﻳﻤﺎن واژﻳﻨﺎل
(P>0/05 ،9/61±0/78اﺧﺘﻼف ﻣﻌﻨﻲداري ﻧﺪاﺷﺖ )ﺟـﺪول .(2ﻫـﻴﭻ
در ﻋﺮض 12ﺳﺎﻋﺖ در 75زن ) (%74/3در ﮔﺮوه ﻣﺤﻠﻮل
ﻣﻮردي از ﻣﺮگ و ﻣﻴﺮ ﻣﺎدري و ﻧﻮزادي وﺟﻮد ﻧﺪاﺷﺖ و ﻣﻴـﺎﻧﮕﻴﻦ دوز
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ و (%25/5) 27زن در ﮔﺮوه واژﻳﻨﺎل رخ داده
ﻣﺼﺮﻓﻲ ﻣﻴﺰوﭘﺮوﺳﺘﻮل 169/7±65/7ﻣﻴﻜﺮوﮔـﺮم ﺑـﻮد .ﺣـﺪاﻛﺜﺮ زﻣـﺎن
ﺑﻮد ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ ﺻﻔﺮ در ﮔﺮوه ﺧﻮراﻛﻲ در ﻣﻘﺎﺑﻞ %11/3در ﮔﺮوه
اﻳﻨﺪاﻛﺸﻦ 24ﺳﺎﻋﺖ ﺑﻮده و در ﺻﻮرت ﻋﺪم ﭘﺎﺳﺦ در 24ﺳﺎﻋﺖ ﭘﺲ
واژﻳﻨﺎل .ﺗﻬﻮع در ﮔﺮوه ﺧﻮراﻛﻲ ﺑﻴﺶﺗﺮ ﺑﻮد .آﭘﮕﺎر ﻛﻢﺗﺮ از ﻫﻔﺖ در
از ﺷﺮوع اﻳﻨﺪاﻛﺸﻦ ،ﺑﺎ ﺗﺸﺨﻴﺺ ﻋﺪم ﭘﺎﺳﺦ زاﻳﻤﺎن ﺳﺰارﻳﻦ اﻧﺠﺎم ﺷﺪ.
دﻗﻴﻘﻪ اول در ﮔﺮوه ﺧﻮراﻛﻲ ﻛﻢﺗﺮ از واژﻳﻨﺎل ﺑﻮد و ﻧﺘﻴﺠﻪ اﻳﻦﻛﻪ ﻣﻴﺰان ﺳﺰارﻳﻦ و ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ در ﮔﺮوه ﻣﺤﻠﻮل ﺧﻮراﻛﻲ ﻛﻪ ﻳﻚ
ﺑﺤﺚ
ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ داﺷﺘﻨﺪ ﻛﻢﺗﺮ از ﮔﺮوه واژﻳﻨﺎل ﺑﻮد و ﻣﺤﻠﻮل
ﺑﺮ اﺳﺎس ﺟﺴﺘﺠﻮي ﻣﺎ ﺗﺎﻛﻨﻮن در ﻛﺸﻮرﻣﺎن اﻳﺮان از ﻣﺤﻠﻮل
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ روﺷﻲ اﻳﻤﻦ و ﻛﺎرا ﺟﻬﺖ اﻟﻘﺎي زاﻳﻤﺎن
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﻪﻋﻨﻮان اﻟﻘﺎي زاﻳﻤﺎن در ﺧﺎﻧﻢﻫﺎي ﺑﺎردار
ﻣﻲﺑﺎﺷﺪ .در ﻣﻄﺎﻟﻌﻪ 11 ،Hofmeyrﺗﺎﺛﻴﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ
اﺳﺘﻔﺎده ﻧﺸﺪه اﺳﺖ .ﻣﻄﺎﻟﻌﺎﺗﻲ در راﺑﻄﻪ ﺑﺎ ﻣﻘﺎﻳﺴﻪ ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﺑﺎ دﻳﻨﻮﭘﺮوﺳﺘﻮن واژﻳﻨﺎل ﻣﻘﺎﻳﺴﻪ ﺷﺪ 695ﺧﺎﻧﻢ ﺑﺎردار ﻛﻪ ﻛﺎﻧﺪﻳﺪ اﻟﻘﺎي
ﺧﻮراﻛﻲ ﺑﺎ واژﻳﻨﺎل ﻳﺎ زﻳﺮ زﺑﺎﻧﻲ در اﻟﻘﺎي زاﻳﻤﺎن در ﺣﺎﻣﻠﮕﻲ ﺗﺮم اﻧﺠﺎم
زاﻳﻤﺎن ﺑﻌﺪ از 34ﻫﻔﺘﮕﻲ ﺷﺪه ﺑﻮدﻧﺪ 346ﻧﻔﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﺷﺪه وﻟﻲ در ﻣﻮرد ﻛﺎراﻳﻲ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ در اﻳﻨﺪاﻛﺸﻦ
ﺧﻮراﻛﻲ )ﻫﺮ دو ﺳﺎﻋﺖ 20gﺗﺎ ﺳﻪ دوز و در ﺻﻮرت ﻧﺎﻣﻨﺎﺳﺐ ﺑﻮدن
ﻛﻪ دوز آن در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﺳﺎﻳﺮ اﺷﻜﺎل آن ﺑﺴﻴﺎر ﻛﻢﺗﺮ اﺳﺖ ﺑﻪﻃﻮري ﻛﻪ
اﻧﻘﺒﺎﺿﺎت ﺑﻪ 40gﻫﺮ دو ﺳﺎﻋﺖ اﻓﺰاﻳﺶ داده ﻣﻲﺷﺪ( و 349ﻧﻔﺮ
از دوز 20ﻣﻴﻜﺮوﮔﺮم در ﺳﺎﻋﺖ در ﭼﻬﺎر ﺳﺎﻋﺖ اول ﺷﺮوع و ﺑﺮ
دﻳﻨﻮﭘﺮوﺳﺘﻮﻧﻮاژﻳﻨﺎل 2mgدر دو دوز ﺑﻪﻓﺎﺻﻠﻪ ﺷﺶ ﺳﺎﻋﺖ درﻳﺎﻓﺖ
اﺳﺎس ﻧﻴﺎز دوز آن ﻗﺎﺑﻞ اﻓﺰاﻳﺶ ﻳﺎ ﻛﺎﻫﺶ اﺳﺖ ﻣﻄﺎﻟﻌﻪاي ﻧﻴﺎﻓﺘﻴﻢ .ﺑﺎ
ﻛﺮدﻧﺪ .ﻫﺪف اﻳﻦ ﻣﻄﺎﻟﻌﻪ زاﻳﻤﺎن واژﻳﻨﺎل در 24ﺳﺎﻋﺖ ﺑﻮد .در ﮔﺮوه
ﺗﻮﺟﻪ ﺑﻪ اﻫﻤﻴﺖ ﻣﻮﺿﻮع ﺑﺮرﺳﻲ ﻣﺎ ﺑﺮ روي ﻣﺎدران ﺑﺎردار ﺑﺎ ﺳﻦ
اول %38و در ﮔﺮوه دوم %36ﺑﻪاﻳﻦ ﻫﺪف دﺳﺖ ﻧﻴﺎﻓﺘﻨﺪ.
ﺑﺎرداري ﺑﻴﺶﺗﺮ از 34ﻫﻔﺘﻪ ﻛﻪ ﻛﺎﻧﺪﻳﺪ ﺧﺘﻢ ﺣﺎﻣﻠﮕﻲ و ﻧﻴﺎز ﺑﻪ اﻟﻘﺎي
ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ ﻛﻪ ﺑﺎﻋﺚ ﺗﻐﻴﻴﺮ
زاﻳﻤﺎن در ﺑﻴﻤﺎرﺳﺘﺎن زﻧﺎن ﺗﻬﺮان از ﺗﺎرﻳﺦ 1388/10/1ﻟﻐﺎﻳﺖ
ﻣﻴﺰوﭘﺮوﺳﺘﻮل و در %3ﮔﺮوه دﻳﻨﻮﭘﺮوﺳﺘﻮن رخ داده ﺑﻮد .رﻳﺴﻚ
1389/10/1داﺷﺘﻨﺪ اﻧﺠﺎم ﺷﺪ .در ﻣﻄﺎﻟﻌﻪ ﺣﺎﺿﺮ ﻧﺸﺎن داده ﺷﺪ ﻛﻪ ﻧﻪ
ﺳﺰارﻳﻦ %16در ﻣﻘﺎﺑﻞ %20ﺑﻮد Outcome .ﺟﻨﻴﻨﻲ در ﻫﺮ دو ﮔﺮوه
ﺗﻨﻬﺎ اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري ﺑﻴﻦ دو ﮔﺮوه از ﻧﻈﺮ ﻋﻮارض داروﻳﻲ،
ﻳﻜﺴﺎن ﺑﻮد .اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻧﺸﺎن داد ﻛﻪ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ
آﭘﮕﺎر ﻧﻮزادان ،ﻧﻮع زاﻳﻤﺎن و رﺿﺎﻳﺖﻣﻨﺪي ﻣﺎدران از داروي ﻣﻮرد
ﺟﻬﺖ اﻟﻘﺎي زاﻳﻤﺎن ﻣﻮﺛﺮ اﺳﺖ و رﻳﺴﻚ ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ آن ﻛﻢ اﺳﺖ.
اﺳﺘﻔﺎده در اﻟﻘﺎي زاﻳﻤﺎن ) (P>0/05وﺟﻮد ﻧﺪاﺷﺖ ﺑﻠﻜﻪ در ﮔﺮوه
اﻟﺒﺘﻪ در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﻛﻪ ﺗﻤﺎم ﻣﺎدران ﺗﺤﺖ ﻣﺎﻧﻴﺘﻮرﻳﻨﮓ ﻗﻠﺒﻲ و اﻧﻘﺒﺎﺿﺎت
ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﻣﺪت زﻣﺎن ﺷﺮوع اﻟﻘﺎ ﺗﺎ زاﻳﻤﺎن واژﻳﻨﺎل
ﺑﻮدﻧﺪ ﻣﻮردي از ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ دﻳﺪه ﻧﺸﺪ ﻛﻪ دﻟﻴﻞ اﺣﺘﻤﺎﻟﻲ آن ﻫﻤﻴﻦ
ﺑﻪﻃﻮر ﻣﻌﻨﻲداري ﻛﻢﺗﺮ ﺷﺪه ﺑﻮد ) .(P=0/001ﻫﻴﭻ ﻣﻮردي از ﻣﺮگ
ﻣﺎﻧﻴﺘﻮرﻳﻨﮓ داﻳﻤﻲ ﺑﻮده ﻛﻪ در ﺻﻮرت اﻓﺰاﻳﺶ اﻧﻘﺒﺎﺿﺎت دوز ﺑﻌﺪي
Cheng
داده ﻧﻤﻲﺷﺪ و در ﺻﻮرت ﺷﺮوع ﻣﺠﺪد اﻟﻘﺎ ،دوز دارو ﺑﻪﻧﺼﻒ ﻛﺎﻫﺶ
10 ،SYﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ در 101زن ﺑﺎردار ﺑﺎ
ﻣﻲﻳﺎﻓﺖ .رﻳﺴﻚ ﺳﺰارﻳﻦ در ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ %16در
ﻣﺎدري و ﻣﺮگ ﻧﻮزادي در دو ﮔﺮوه وﺟﻮد ﻧﺪاﺷﺖ .در ﻣﻄﺎﻟﻌﻪ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
FHR
ﺷﺪه ﺑﻮد در %4ﮔﺮوه
ﻣﻘﺎﻳﺴﻪ اﺛﺮ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ در اﻟﻘﺎي زاﻳﻤﺎن در زﻧﺎن ﺑﺎ ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ
417
ﻣﻘﺎﺑﻞ %26در ﮔﺮوه اﻛﺴﻲﺗﻮﺳﻴﻦ در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﺑﻮد .در ﻣﻄﺎﻟﻌﻪ
ﺳﺎﻋﺖ اول و ﻣﺘﻮﺳﻂ ﻓﺎﺻﻠﻪ زﻣﺎﻧﻲ ﺑﻴﻦ ﺷﺮوع اﻟﻘﺎ ﺗﺎ زاﻳﻤﺎن واژﻳﻨﺎل
12 Matonhodze BBﻣﻘﺎﻳﺴﻪ ﺳﻪ ﻣﺘﺪ ﺟﻬﺖ اﻟﻘﺎ در ﺧﺎﻧﻢﻫﺎي ﺑﺎردار
ﺑﻮد .ﻫﺪف ﺛﺎﻧﻮﻳﻪ ﺷﺎﻣﻞ ﻧﻴﺎز ﺑﻪﺗﻘﻮﻳﺖ اﻟﻘﺎ ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ ،دوز ﺗﻮﺗﺎل
ﺑﺎ ﻣﺎﻣﺒﺮان ﺳﺎﻟﻢ ﺷﺪه ﺑﻮد -1اﻛﺴﺘﺮاآﻣﻨﻴﻮﺗﻴﻚ ﻓﻮﻟﻲ ﻛﺎﺗﺘﺮ ﺑﻪﻫﻤﺮاه
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ،ﺗﻌﺪاد زاﻳﻤﺎن ﺳﺰارﻳﻦ ،ﺷﻜﺴﺖ اﻟﻘﺎ ،ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ
ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل در 174زن -2 ،ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ
رﺣﻤﻲ و اوتﻛﺎم ﺟﻨﻴﻨﻲ ﺑﻮد .ﻧﺘﻴﺠﻪ اﻳﻦ ﻣﻄﺎﻟﻌﻪ %97/4در 24ﺳﺎﻋﺖ
ﺑﻪﺗﻨﻬﺎﻳﻲ در 176زن -3 ،دﻳﻨﻮﭘﺮوﺳﺘﻮن واژﻳﻨﺎل در 176زن .ﻫﺪف
اول وارد اﻛﺘﻴﻮ ﻓﺎز ﺷﺪﻧﺪ و %93/5در 24ﺳﺎﻋﺖ اول زاﻳﻤﺎن واژﻳﻨﺎل
اوﻟﻴﻪ در اﻳﻦ ﺳﻪ ﻣﺘﺪ زاﻳﻤﺎن واژﻳﻨﺎل در 24ﺳﺎﻋﺖ اول ﺑﻮد ﻛﻪ در ﻫﺮ
داﺷﺘﻨﺪ .ﻣﺘﻮﺳﻂ ﻓﺎﺻﻠﻪ زﻣﺎﻧﻲ 7/9ﺳﺎﻋﺖ ﺑﻮد .ﻣﺘﻮﺳﻂ و ﻣﻴﺎﻧﮕﻴﻦ دوز
ﺳﻪ ﮔﺮوه ﻣﺸﺎﺑﻪ ﺑﻮد .زاﻳﻤﺎن ﺳﺰارﻳﻦ ،اﺳﺘﻔﺎده از وﻛﻴﻮم و ﻧﻴﺎز ﺑﻪ
ﻣﺼﺮﻓﻲ ﻣﻴﺰوﭘﺮوﺳﺘﻮل 206ﻣﻴﻜﺮوﮔﺮم ﺑﻮد .ﻫﺸﺖ ﻧﻔﺮ ﻧﻴﺎز ﺑﻪ
ﺗﻘﻮﻳﺖ اﻟﻘﺎ در ﮔﺮوه اول ﺑﻴﺶﺗﺮ ﺑﻮد وﻟﻲ اﻳﻦ اﺧﺘﻼف ﻣﻌﻨﻲدار ﻧﺒﻮد.
اﻛﺴﻲﺗﻮﺳﻴﻦ ﭘﻴﺪا ﻛﺮدﻧﺪ و ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ دﻳﺪه ﻧﺸﺪ .اﻳﻦ ﻣﻄﺎﻟﻌﻪ
ﻋﻮارض ﺟﺎﻧﺒﻲ و ﻋﻮارض ﺟﻨﻴﻨﻲ در ﻫﺮ ﺳﻪ ﮔﺮوه ﻣﺸﺎﺑﻪ ﺑﻮد و اﺿﺎﻓﻪ
ﻧﺸﺎن داد ﻛﻪ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﻳﻚ روش اﻳﻤﻦ و ﻣﻮﺛﺮ
ﻛﺮدن ﻓﻮﻟﻲ ﻛﺎﺗﺘﺮ اﺛﺮ ﻣﻔﻴﺪي در ﺑﺮاﺑﺮ ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺗﻨﻬﺎ ﻳﺎ
در اﻟﻘﺎي زاﻳﻤﺎن ﻣﻲﺑﺎﺷﺪ و دوز آن ﻗﺎﺑﻞ ﺗﻨﻈﻴﻢ اﺳﺖ .در ﺑﺮرﺳﻲ ﻣﺎ
دﻳﻨﻮﭘﺮوﺳﺘﻮن ﻧﺪارد .اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻫﻢ ﻧﺸﺎن داد ﻛﻪ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﻣﺘﻮﺳﻂ ﻓﺎﺻﻠﻪ زﻣﺎﻧﻲ 11/07ﺳﺎﻋﺖ و ﻣﻴﺎﻧﮕﻴﻦ دوز ﻣﺼﺮﻓﻲ
ﺧﻮراﻛﻲ ﺟﻬﺖ اﻟﻘﺎي زاﻳﻤﺎن ﻣﻮﺛﺮ اﺳﺖ و اﺿﺎﻓﻪ ﻛﺮدن ﻓﻮﻟﻲ ﻛﺎﺗﺘﺮ در
ﻣﻴﺰوﭘﺮوﺳﺘﻮل 170ﻣﻴﻜﺮوﮔﺮم ﺑﻮد و %84در 24ﺳﺎﻋﺖ زاﻳﻤﺎن
آﻣﺎده ﻛﺮدن ﺳﺮﻳﻜﺲ ﻛﻤﻚ ﭼﻨﺪاﻧﻲ ﻧﻜﺮده و ﻣﻲﺗﻮان از ﻣﺤﻠﻮل
واژﻳﻨﺎل داﺷﺘﻨﺪ و ﺑﻌﺪ از 24ﺳﺎﻋﺖ ﺑﺎ ﺗﺸﺨﻴﺺ ﻋﺪم ﭘﺎﺳﺦ ﺑﻪ
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﻪﺗﻨﻬﺎﻳﻲ ،ﻫﻤﺎﻧﻨﺪ آنﭼﻪ در ﻣﻄﺎﻟﻌﻪ ﻣﺎ اﻧﺠﺎم
اﻳﻨﺪاﻛﺸﻦ ،ﺳﺰارﻳﻦ ﻣﻲﺷﺪﻧﺪ .در ﻣﻄﺎﻟﻌﻪاي در ﺑﻴﻤﺎرﺳﺘﺎن
13
Jahannesburgدر آﻓﺮﻳﻘﺎي ﺟﻨﻮﺑﻲ 16در 25زن از ﻣﺤﻠﻮل
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ) 100gﻫﺮ ﭼﻬﺎر ﺳﺎﻋﺖ ﺗﺎ ﺷﺶ دوز( ﺑﺎ
ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﻫﺮ دو ﺳﺎﻋﺖ 20gﺗﺎ ﺳﻪ دوز و ﺑﻌﺪ ﺑﻪ 40g
اﻛﺴﻲﺗﻮﺳﻴﻦ ورﻳﺪي ﺟﻬﺖ اﻟﻘﺎي زاﻳﻤﺎن در زﻧﺎن ﺑﺎ ﺳﺮوﻳﻜﺲ ﻣﻨﺎﺳﺐ
اﻓﺰاﻳﺶ داده ﻣﻲﺷﺪ اﺳﺘﻔﺎده ﺷﺪ 18 .ﻧﻔﺮ در ﻋﺮض 32ﺳﺎﻋﺖ زاﻳﻤﺎن
)ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب < (6ﻣﻘﺎﻳﺴﻪ ﺷﺪ .ﻧﺘﻴﺠﻪ اﻳﻦ ﻣﻄﺎﻟﻌﻪ اﻳﻦ ﺑﻮد ﻛﻪ
واژﻳﻨﺎل ﻛﺮد و دو ﻧﻔﺮ دﭼﺎر ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ ﺷﺪ و ﺳﺰارﻳﻦ در %20
در ﻣﻮارديﻛﻪ ﺳﺮوﻳﻜﺲ ﻣﻨﺎﺳﺐ اﺳﺖ ﻣﻴﺰوﭘﺮوﺳﺘﻮل ارﺟﺤﻴﺘﻲ ﻧﺪارد و
رخ داد .در ﻣﻄﺎﻟﻌﻪ Dällenbach Pدوز ﻛﻢ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﻋﻮارض ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ آن ﺑﻴﺶﺗﺮ اﺳﺖ و اﺣﺘﻤﺎل ﭘﺎرﮔﻲ رﺣﻤﻲ
ﺧﻮراﻛﻲ ﺑﺎ دﻳﻨﻮﭘﺮوﺳﺘﻮن واژﻳﻨﺎل ﺟﻬﺖ Ripeningﺳﺮوﻳﻜﺲ و اﻟﻘﺎي
دارد .اﻟﺒﺘﻪ در اﻳﻦ ﻣﻄﺎﻟﻌﻪ از دوز ﺑﺎﻻي ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ اﺳﺘﻔﺎده
زاﻳﻤﺎن در ﺧﺎﻧﻢﻫﺎي ﺑﺎ ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب > 6ﻣﻘﺎﻳﺴﻪ ﺷﺪ.
17
ﺷﺪه وﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب < 6ﻣﻲﺑﺎﻳﺴﺖ از دوز
ﺳﺰارﻳﻦ در دو ﮔﺮوه ﺑﻪﺗﺮﺗﻴﺐ %18و %19ﺑﻮد .ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ %9در
ﻛﻢﺗﺮ اﺳﺘﻔﺎده ﻣﻲﺷﺪ ﺗﺎ ﺧﻄﺮ ﭘﺎرﮔﻲ رﺣﻤﻲ از ﺑﻴﻦ ﺑﺮود .در ﻣﻄﺎﻟﻌﻪ ﻣﺎ
ﺑﺮاﺑﺮ %14و Outcomeﺟﻨﻴﻨﻲ ﺗﻔﺎوﺗﻲ ﻧﺪاﺷﺖ .در اﻳﻦ ﻣﻄﺎﻟﻌﻪ اﺧﺘﻼﻓﻲ
ﺑﺮ ﺧﻼف ﻣﻄﺎﻟﻌﻪ ﺣﺎﺿﺮ ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب > 6ﺑﻮد و ﺑﺎ اﻳﻦ
ﺑﻴﻦ دو روش دوز ﻛﻢﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل ﺧﻮراﻛﻲ ﺑﺎ دﻳﻨﻮﭘﺮوﺳﺘﻮن
ﺷﺮاﻳﻂ از دوز ﺑﺴﻴﺎر ﻛﻢﺗﺮ 20gاﺳﺘﻔﺎده ﺷﺪ و ﻫﻴﭻ ﻣﻮردي از
واژﻳﻨﺎل ﺟﻬﺖ Ripeningﺳﺮوﻳﻜﺲ وﺟﻮد ﻧﺪاﺷﺖ .ﺑﺎ ﺑﺮرﺳﻲ و
Zateroglu
ﻣﻘﺎﻳﺴﻪ اﻳﻦ ﻣﻄﺎﻟﻌﺎت و ﻣﻄﺎﻟﻌﻪ ﺣﺎﺿﺮ ﻣﻲﺗﻮان ﭼﻨﻴﻦ اﺳﺘﻨﺒﺎط ﻛﺮد ﻛﻪ
اﻳﻤﻨﻲ و ﻛﺎراﻳﻲ ﻣﻴﺰوﭘﺮوﺳﺘﻮل واژﻳﻨﺎل ﺑﺎ اﻛﺴﻲﺗﻮﺳﻴﻦ ﺟﻬﺖ رﻳﭗ
درﺻﻮرت وﺟﻮد داﺷﺘﻦ ﻣﻌﻴﺎرﻫﺎي ورود و ﻧﺪاﺷﺘﻦ ﻣﻌﻴﺎرﻫﺎي ﺧﺮوﺟﻲ
ﺷﺪن ) (Ripeningﺳﺮوﻳﻜﺲ در زﻧﺎن دﭼﺎر ﭘﺎرﮔﻲ زودرس ﻏﺸﺎﻫﺎي
)ﻫﻤﺎنﻃﻮر ﻛﻪ در ﻣﺘﻦ ذﻛﺮ ﺷﺪ( ،ﻣﻲﺗﻮان ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل
14
ﺧﻮراﻛﻲ را ﺟﺎﻳﮕﺰﻳﻦ ﺳﺎﻳﺮ روشﻫﺎي ﻓﺎرﻣﺎﻛﻮﻟﻮژﻳﻚ ﻣﺜﻞ
ﻧﺘﺎﻳﺞ زاﻳﻤﺎن واژﻳﻨﺎل و ﺳﺰارﻳﻦ و آﭘﮕﺎر در ﻫﺮ دو ﮔﺮوه ﻣﺸﺎﺑﻪ ﺑﻮد .در
دﻳﻨﻮﭘﺮوﺳﺘﻮن ،اﻛﺴﻲﺗﻮﺳﻴﻦ و ﺳﺎﻳﺮ روشﻫﺎي ﻣﺼﺮﻓﻲ ﻣﻴﺰوﭘﺮوﺳﺘﻮل
ﻣﻄﺎﻟﻌﻪ 77 ،Cheng SYﺧﺎﻧﻢ ﺑﺎردار ) 37ﻧﻮﻟﻲﭘﺎر و 40ﻣﻮﻟﺘﻲﭘﺎر( ﻛﻪ
اﻋﻢ از ﺧﻮراﻛﻲ ،زﻳﺮ زﺑﺎﻧﻲ و واژﻳﻨﺎل ﻛﺮد ﭼﻮن ﻫﻢ دوز آن ﻛﻢﺗﺮ اﺳﺖ
ﻛﺎﻧﺪﻳﺪ اﻟﻘﺎي زاﻳﻤﺎن ﺑﻌﺪ از ﻫﻔﺘﻪ 37ﺑﺎرداري ﺑﺎ ﺳﺮوﻳﻜﺲ ﻧﺎﻣﻨﺎﺳﺐ
وﻫﻢ روش اﺳﺘﻔﺎده آن آﺳﺎنﺗﺮ اﺳﺖ و ﻛﺎراﻳﻲ و اﻳﻤﻨﻲ آن در اﻟﻘﺎي
ﻣﻌﻴﺎر ﻧﻤﺮهدﻫﻲ ﺑﻴﺸﺎب > 7ﺑﻮدﻧﺪ ﺗﺤﺖ اﻟﻘﺎ ﺑﺎ ﻣﺤﻠﻮل ﻣﻴﺰوﭘﺮوﺳﺘﻮل
زاﻳﻤﺎن ﻣﺸﺎﺑﻪ و ﺣﺘﻲ در ﺑﻌﻀﻲ ﻣﻄﺎﻟﻌﺎت ﺑﻬﺘﺮ از ﺳﺎﻳﺮ روشﻫﺎي
ﻗﺮار ﮔﺮﻓﺘﻨﺪ 15.ﻫﺪف اوﻟﻴﻪ در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺗﻌﺪاد زاﻳﻤﺎن واژﻳﻨﺎل در 24
ﻓﺎرﻣﺎﻛﻮﻟﻮژﻳﻚ ﻣﺜﻞ دﻳﻨﻮﭘﺮوﺳﺘﻮن و اﻛﺴﻲﺗﻮﺳﻴﻦ ﺑﻮده اﺳﺖ.
ﺷﺪه ﺟﻬﺖ اﻳﻨﺪاﻛﺸﻦ اﺳﺘﻔﺎده ﻛﺮد .در ﻣﻄﺎﻟﻌﻪ
Wing DA
ﻫﻴﭙﺮاﺳﺘﻴﻤﻮﻟﻴﺸﻦ و ﭘﺎرﮔﻲ رﺣﻤﻲ دﻳﺪه ﻧﺸﺪ .در ﻣﻄﺎﻟﻌﻪ
ﺟﻨﻴﻨﻲ
)(PROM
ﻛﻪ در زﻣﺎن ﺗﺮم ﻣﺮاﺟﻌﻪ ﻛﺮده ﺑﻮدﻧﺪ ﻣﻘﺎﻳﺴﻪ ﺷﺪ.
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻫﻤﻜﺎران ﻧﻴﺮوﻣﻨﺶ و Niroomanesh Sh.ﺷﻴﺮﻳﻦ et al.
418
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10. Cheng SY, Ming H, Lee JC. Titrated oral compared with vaginal misoprostol for labor induction: a randomized controlled trial. Obstet Gynecol 2008;111(1):119-25. 11. Hofmeyr GJ, Alfirevic Z, Matonhodze B, Brocklehurst P, Campbell E, Nikodem VC. Titrated oral misoprostol solution for induction of labour: a multi-centre, randomised trial. BJOG 2001;108(9):952-9. 12. Matonhodze BB, Hofmeyr GJ, Levin J. Labour induction at term: a randomised trial comparing Foley catheter plus titrated oral misoprostol solution, titrated oral misoprostol solution alone, and dinoprostone. S Afr Med J 2003;93(5):375-9. 13. Wing DA, Fassett MJ, Guberman C, Tran S, Parrish A, Guinn D. A comparison of orally administered misoprostol to intravenous oxytocin for labor induction in women with favorable cervical examinations. Am J Obstet Gynecol 2004;190(6):1689-94; discussion 1694-6. 14. Zeteroğlu S, Engin-Ustün Y, Ustün Y, Güvercinçi M, Sahin G, Kamaci M. A prospective randomized study comparing misoprostol and oxytocin for premature rupture of membranes at term. J Matern Fetal Neonatal Med 2006;19(5):283-7. 15. Cheng SY, Chen TC. Pilot study of labor induction with titrated oral misoprostol. Taiwan J Obstet Gynecol 2006;45(3):225-9. 16. Hofmeyr GJ, Matonhodze BB, Alfirevic Z, Campbell E, de Jager M, Nikodem C. Titrated oral misoprostol solution: a new method of labour induction. S Afr Med J 2001;91(9):775-6. 17. Dällenbach P, Boulvain M, Viardot C, Irion O. Oral misoprostol or vaginal dinoprostone for labor induction: a randomized controlled trial. Am J Obstet Gynecol 2003;188(1):162-7.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
Tehran University Medical Journal; Vol. 69, No. 7, October 2011: 413-419
Titrated oral misoprostol solution compared with oxytocin for induction of labor in women with unfavorable cervix
Shirin Niroomanesh M.D.1 Masoumeh Dadashaliha M.D.2* Mina Akrami M.D.2 1- Department of Perinatology, Tehran University of Medical Sciences, Tehran, Iran. 2- Department of Obstetrics and Gynecology, Women Hospital (Mirza Koochackkhan), Tehran University of Medical Sciences, Tehran, Iran.
Abstract
Received: June 01, 2011 Accepted: June 27, 2011
Background: Uterine contractions and an appropriate cervix are two important factors in labor contributing to good pregnancy outcomes. Oxytocin and prostaglandins, such as misoprostol, are used for the induction of labor. Misoprostol is used for cervical ripening and labor induction. The aim of this trial was to compare the efficacy and safety of titrated oral misoprostol solution with oxytocin for labor induction in pregnant women with an unfavorable cervix. Methods: In this randomized double-blind clinical trial, 140 women with a gestational age of 34−42 weeks and an unfavorable cervix were recruited. The participants had an indication for labor induction and had been referred to the Women’s Hospital in Tehran, Iran between January 2010 and January 2011. The participants were randomly assigned to receive 20 µg/hour titrated oral misoprostol plus intravenous placebo or 6 mU/min oxytocin plus oral placebo. In case contractions were inadequate, the drug doses were gradually increased. Pharmacological complications, the mean interval from the start of induction till vaginal delivery and delivery type were monitored and analyzed in both groups. Results: The mean interval from the start of induction till vaginal delivery in misoprostol group was shorter than the oxytocin group (11.07±3.42 vs. 14.87±3.21 hours, P=0.001). The frequency of pharmacological complications and vaginal or cesarean
deliveries were similar between the two groups (P>0.05). Conclusion: Use of titrated oral misoprostol is a safe and effective method for labor induction in pregnant women with unfavorable cervix. Misoprostol is associated with a shorter interval from induction to vaginal delivery than oxytocin. *
Corresponding author: Dept. of Obstetrics and Gynecology, Women Hospital (Mirza Koochackkhan), Karimkhan Ave., Tehran, Iran. Tel: +98-21-88900002 E-mail: dadashaliha@razi.tums.ac.ir
Keywords: Cervix, induction, labor, misoprostol, oxytocin.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
420-425 ،1390 ﻋﺮوقﻣﻬﺮ ﺷﻤﺎره ،7 ﺗﺤﺖ، 69 دوره درديﻲدرﺗﻬﺮان، ﺑﻲﭘﺰﺷﻜ ﻋﻠﻮم داﻧﺸﮕﺎه ﺪه ﭘﺰﺷﻜﻲ، ﻣﺠﻠﻪ داﻧﺸﻜ ﺗﺤﺘﺎﻧﻲ اﻧﺪام ﺟﺮاﺣﻲ ﺑﻴﻤﺎران ﻣﺪت ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ و ﺗﻐﻴﻴﺮات
ﻣﻘﺎﻳﺴﻪ دو روش ﺑﻲﺣﺴﻲ ﻧﺨﺎﻋﻲ در ﺣﺎﻟﺖﻫﺎي ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و ﻧﺸﺴﺘﻪ در ﺟﺮاﺣﻲ ﻋﺮوق اﻧﺪام ﺗﺤﺘﺎﻧﻲ
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1390/02/14 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/04/13 :
ﭼﻜﻴﺪه
1
ﻣﺤﻤﺪرﺿﺎ ﻣﻬﺎﺟﺮ
*1
زﻣﻴﻨﻪ و ﻫﺪف :ﺑﻴﻤﺎران ﺗﺤﺖ ﻋﻤﻞ ﺟﺮاﺣﻲ ﻋﺮوﻗﻲ اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﻛﻪ ﺗﻮﺳﻂ ﺟﺮاﺣﺎن ﻣﺘﺒﺤﺮ ﻋﺮوق ﺗﺤﺖ ﻋﻤﻞ ﺟﺮاﺣﻲ
1
ﻗﺮار ﻣﻲﮔﻴﺮﻧﺪ از ﻟﺤﺎظ ﺗﻤﻬﻴﺪات ﺑﻴﻬﻮﺷﻲ ﺑﺴﻴﺎر ﭘﺮﺧﻄﺮ ﺗﻠﻘﻲ ﻣﻲﮔﺮدﻧﺪ .در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻣﻘﺎﻳﺴﻪ دو روش ﺑﻲﺣﺴﻲ
1
ﻧﺨﺎﻋﻲ در ﺣﺎﻟﺖﻫﺎي ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و ﻧﺸﺴﺘﻪ از ﻧﻈﺮ ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ و ﻣﺪت ﺑﻲدردي در ﺑﻴﻤﺎران ﺗﺤﺖ ﺟﺮاﺣﻲ
ﻛﺴﺮي ﻛﺮوﻧﺪﻳﺎن زاﻫﺪ ﺣﺴﻴﻦﺧﺎن اﻓﺸﻴﻦ ﺟﻌﻔﺮزاده
ﻋﺮوق اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺗﻮﺳﻂ داروي ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ) (%0/5ﻫﻴﭙﺮﺑﺎر ﺻﻮرت ﭘﺬﻳﺮﻓﺘﻪ اﺳﺖ .روش ﺑﺮرﺳﻲ :ﺑﺮاي
2
ﺳﻬﻴﻼ دﺑﻴﺮان
40ﺑﻴﻤﺎر ﻛﻪ ﺑﻪ دو ﮔﺮوه 20ﻧﻔﺮه ﺗﻘﺴﻴﻢﺑﻨﺪي ﺷﺪﻧﺪ در دو ﺣﺎﻟﺖ ﻧﺸﺴﺘﻪ ) (Sitting positionو ﺣﺎﻟﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ -1ﮔﺮوه ﺑﻴﻬﻮﺷﻲ و ﻣﺮاﻗﺒﺖﻫﺎي وﻳﮋه ،ﺑﻴﻤﺎرﺳﺘﺎن اﻣﺎمﺧﻤﻴﻨﻲ )ره(
)(Lateral position
ﺑﻲﺣﺴﻲ ﺑﻴﻤﺎران
-2ﮔﺮوه ﭘﺰﺷﻜﻲ اﺟﺘﻤﺎﻋﻲ
داروي ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ﻫﻴﭙﺮﺑﺎر %0/5ﺑﻪﻣﻴﺰان
T10
3ml
در ﻓﻀﺎي ﺳﺎب آراﻛﻨﻮﻳﻴﺪ ﺗﺰرﻳﻖ ﮔﺮدﻳﺪ .ﺳﻄﺢ
در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪ و ﻧﺘﺎﻳﺞ از ﻧﻈﺮ ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ و ﻣﺪت ﺑﻲدردي در دو ﮔﺮوه ﻣﻘﺎﻳﺴﻪ ﺷﺪ.
ﻳﺎﻓﺘﻪﻫﺎ :اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري ﺑﻴﻦ ﺗﻐﻴﻴﺮات ﻓﺸﺎر ﺧﻮن ﻣﺘﻮﺳﻂ ﺷﺮﻳﺎﻧﻲ ،ﻓﺸﺎر ﺧﻮن ﺳﻴﺴﺘﻮﻟﻴﻚ و ﻓﺸﺎر ﺧﻮن
داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان.
دﻳﺎﺳﺘﻮﻟﻴﻚ دو ﮔﺮوه وﺟﻮد داﺷﺖ ) .(P<0/05اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري ﺑﻴﻦ ﺗﻐﻴﻴﺮات ﺿﺮﺑﺎن ﻗﻠﺐ در ﻛﻠﻴﻪ زﻣﺎنﻫﺎي ﻣﻮرد ﺑﺮرﺳﻲ در دو ﮔﺮوه وﺟﻮد داﺷﺖ )(P<0/05؛ اﻣﺎ در ﻣﻮرد ﺿﺮﺑﺎن ﻗﻠﺐ در دﻗﺎﻳﻖ ﻧﺨﺴﺖ و ﺳﻲام اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري را ﺑﻴﻦ دو ﮔﺮوه ﻧﺸﺎن ﻧﻤﻲداد ) .(P>0/05ﻃﻮل ﺑﻲﺣﺴﻲ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﺑﻪﻣﻴﺰان ﻣﻌﻨﻲداري ﻃﻮﻻﻧﻲﺗﺮ و ﻣﻴﺰان ﻣﺎﻳﻊ ﻣﺼﺮﻓﻲ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺑﻪﻣﻴﺰان ﻣﻌﻨﻲداري ﺑﻴﺸﺘﺮ ﺑﻮد ) .(P<0/05ﻧﺘﻴﺠﻪﮔﻴﺮي :در ﻣﺠﻤﻮع ﺑﺮ
*
اﺳﺎس ﻧﺘﺎﻳﺞ ﺣﺎﺻﻞ از اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﭼﻨﻴﻦ اﺳﺘﻨﺒﺎط ﻣﻲﺷﻮد ﻛﻪ ﻣﻴﺰان ﺗﻐﻴﻴﺮات ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ در ﺑﻴﻬﻮﺷﻲ اﺳﭙﺎﻳﻨﺎل ﺑﺎ ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﺗﻬﺮان ،ﺑﻠﻮار ﻛﺸﺎورز ،ﺑﻴﻤﺎرﺳﺘﺎن
اﻣﺎمﺧﻤﻴﻨﻲ)ره( ،ﮔﺮوه ﺑﻴﻬﻮﺷﻲ و ﻣﺮاﻗﺒﺖﻫﺎي وﻳﮋه
ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ در ﭘﻮزﻳﺸﻦ ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﻛﻢﺗﺮ از ﻧﺸﺴﺘﻪ ﻣﻲﺑﺎﺷﺪ.
ﺗﻠﻔﻦ021-88249920 : E-mail: kassramail@yahoo.com
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ،ﺑﻴﻬﻮﺷﻲ ،اﺳﭙﺎﻳﻨﺎل ،ﭘﻮزﻳﺸﻦ ،ﺟﺮاﺣﻲﻫﺎي اﻧﺪام ﺗﺤﺘﺎﻧﻲ.
ﻣﻘﺪﻣﻪ
ﻋﻤﻞ ﺟﺮاﺣﻲ ﻗﺮار ﺧﻮاﻫﻨﺪ ﮔﺮﻓﺖ و ﺑﻪﻃﻮر ﻋﻤﺪه از ﻋﺮوق ﻟﮕﻨﻲ اﺻﻠﻲ ﺑﻪ ﻋﺮوق اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺑﺎيﭘﺲ ﻣﻲﮔﺮدد ،ﺑﺎﻳﺪ ﺑﺎ ﻛﻢﺗﺮﻳﻦ ﺧﻄﺮ و
ﺑﻴﻤﺎران ﻧﻴﺎزﻣﻨﺪ ﺑﻪ ﺗﺮﻣﻴﻢ و اﺻﻼح ﺑﻴﻤﺎريﻫﺎي ﻋﺮوﻗﻲ اﻧﺪام ﺗﺤﺘﺎﻧﻲ
ﻋﺎرﺿﻪاي ﻫﻤﺮاه ﺑﺎﺷﺪ 3.ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺑﻴﻤﺎريﻫﺎي ﻫﻤﺮاه در اﻳﻦ ﺑﻴﻤﺎران
ﻛﻪ ﻋﻤﻮﻣﺎً ﺗﻮﺳﻂ ﺟﺮاﺣﺎن ﻣﺘﺒﺤﺮ ﻋﺮوق و ﺑﺎ ﻛﻤﻚ از ﭘﺮوﺗﺰﻫﺎي
ﻛﻪ ﻋﻼوه ﺑﺮ ﺳﻴﺴﺘﻢ ﻗﻠﺐ و ﻋﺮوق و ﮔﺎﻫﻲ ﺳﻴﺴﺘﻢ ﺗﻨﻔﺴﻲ ،ﻛﻠﻴﻪﻫﺎ و
ﻋﺮوﻗﻲ ﺧﻮنرﺳﺎﻧﻲ اﻧﺪام ﺗﺤﺘﺎﻧﻲ اﻳﺸﺎن ﺗﺎﻣﻴﻦ ﻣﻲﮔﺮدد از ﻟﺤﺎظ
ﺳﺎﻳﺮ ارﮔﺎنﻫﺎ را ﻧﻴﺰ درﮔﻴﺮ ﻧﻤﻮده اﺳﺖ ،ﻛﻢ ﻛﺮدن ﺗﻐﻴﻴﺮات
ﺗﻤﻬﻴﺪات ﺑﻴﻬﻮﺷﻲ ﺑﺴﻴﺎر ﭘﺮﺧﻄﺮ ﺗﻠﻘﻲ ﻣﻲﮔﺮدﻧﺪ 1.ﺑﺪﻳﻬﻲ اﺳﺖ ﻛﻪ
ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ در ﻃﻲ ﺑﻴﻬﻮﺷﻲ از ﺣﺴﺎﺳﻴﺖ ﺑﺴﻴﺎر ﺑﺎﻻﻳﻲ ﺑﺮﺧﻮردار
ﺑﻴﻤﺎريﻫﺎي ﺳﻴﺴﺘﻤﻴﻚ ﭘﻴﺸﺮﻓﺘﻪاي ﻛﻪ ﺳﻴﺴﺘﻢ ﻗﻠﺐ و ﻋﺮوق اﻳﻦ
اﺳﺖ 4.ﻣﺤﺪودﻳﺖ در ﻣﺼﺮف دارو و ﻫﻢﭼﻨﻴﻦ ﻛﺎﻫﺶ ﻋﻮارض
ﺑﻴﻤﺎران را ﻃﻲ ﺳﺎلﻫﺎ ﺑﻴﻤﺎري درﮔﻴﺮ ﻧﻤﻮده اﺳﺖ ﻧﺸﺎﻧﮕﺎن ﺧﻮد را
ﺗﺮوﻣﺒﻮآﻣﺒﻮﻟﻴﻚ ﭘﺲ از ﺟﺮاﺣﻲ از ﻣﺰاﻳﺎي ﺑﻴﻬﻮﺷﻲ ﻧﺎﺣﻴﻪاي ﺑﺮاي
ﺑﻪﺻﻮرت ﻧﺎرﺳﺎﻳﻲ در ﺧﻮنرﺳﺎﻧﻲ ،ﺳﻴﺎه ﺷﺪن اﻧﺪامﻫﺎ و ﺗﻮرم و درد و
ﺟﺮاﺣﻲ اﻳﻦ ﺑﻴﻤﺎران ﻣﻲﺑﺎﺷﺪ 5.اﻳﻦ روش ﺑﻪﻋﻠﺖ ﺑﻠﻮك ﻧﺎﺣﻴﻪاي در
اﻳﺠﺎد ﺧﻄﺮات ﻣﻬﻤﻲ ﻣﺎﻧﻨﺪ ﺗﺮﻣﺒﻮز ﻋﺮوﻗﻲ ﻧﺸﺎن ﻣﻲدﻫﺪ 2.اﻧﺘﺨﺎب
اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺗﻨﻬﺎ ﺳﻴﺴﺘﻢ ﻋﺼﺒﻲ ﺣﺴﻲ ﺣﺮﻛﺘﻲ را ﺑﻠﻮك ﻧﻤﻮده و ﺑﺎ
روش ﺑﻴﻬﻮﺷﻲ ﻣﻨﺎﺳﺐ ﺑﺮاي اﻳﻦ ﺑﻴﻤﺎران ﻛﻪ ﺑﻪﻣﺪت 2-3ﺳﺎﻋﺖ ﺗﺤﺖ
ﻛﺎﻫﺶ واﺿﺢ در ﺗﻮﻧﻴﺴﻴﺘﻪ ﻋﺮوﻗﻲ ﻣﻲﺗﻮاﻧﺪ ﺧﻮنرﺳﺎﻧﻲ اﻧﺪام ﺗﺤﺘﺎﻧﻲ را
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻣﺤﻤﺪرﺿﺎ ﻣﻬﺎﺟﺮ و ﻫﻤﻜﺎران
ﺑﻪﻃﻮر ﻣﻮﺛﺮي ﺑﻬﺒﻮد ﺑﺨﺸﺪ ،از ﻃﺮف دﻳﮕﺮ ﻛﻢﺗﺮﻳﻦ اﺛﺮ ﻣﺴﺘﻘﻴﻢ را ﺑﺮ
421
) %0/5 (Merck, Germanyﺑﻪﻣﻴﺰان 3mlﺗﺰرﻳﻖ ﮔﺮدﻳﺪ و ﺳﻄﺢ T10
در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪ .در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺑﻴﻤﺎران
روي ﻗﻠﺐ رﻳﻪ و ﻣﻐﺰ داﺷﺘﻪ و ﺑﺎ ﻛﺎﻫﺶ ﻣﻘﺎوﻣﺖ ﺑﺮ ﺳﺮ راه ﺑﺮونده
ﺑﻲﺣﺴﻲ ﺑﻴﻤﺎران در
ﻗﻠﺒﻲ ﻗﺪرت ﭘﻤﭗ و اﻧﺪﻛﺲ ﻗﻠﺒﻲ را ﻧﻴﺰ ﺑﻬﺒﻮد ﻣﻲﺑﺨﺸﺪ 6.اﻳﻦ ﺑﻴﻤﺎران
ﭘﺲ از اﻧﺠﺎم ﺗﻜﻨﻴﻚ ﺑﺎ ﺳﻮزن اﺳﭙﺎﻳﻨﺎل 25ﺑﻪ ﭘﺸﺖ ﺧﻮاﺑﺎﻧﺪه ﺷﺪه و
ﻋﻤﺪﺗﺎ در ﺳﻨﻴﻦ ﻣﻴﺎنﺳﺎل و ﻣﺴﻦ ﺑﻮده و ﻣﺸﻜﻼﺗﻲ ﻣﺎﻧﻨﺪ ﺑﺮوﻧﺸﻴﺖ،
ﭘﺲ از اﺳﺘﻘﺮار ﺑﻠﻮك اﺟﺎزه آﻏﺎز ﻋﻤﻞ ﺟﺮاﺣﻲ داده ﺷﺪ .در ﺑﻴﻤﺎران
ﺑﻴﻤﺎريﻫﺎي اﻧﺴﺪادي رﻳﻮي ،دﻳﺎﺑﺖ ،ﺑﻴﻤﺎريﻫﺎي ﻋﺮوﻗﻲ ﻣﺎﻧﻨﺪ ﺑﻮرﮔﺮ
ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﻧﻴﺰ ﭘﺲ از ﺧﻮاﺑﺎﻧﻴﺪن ﺑﻴﻤﺎران ﺑﻪﺳﻤﺖ اﻧﺪام ﻣﻮرد ﻋﻤﻞ
را ﺑﻪﻫﻤﺮاه ﺧﻮد دارﻧﺪ 7.از ﻃﺮف دﻳﮕﺮ اﻳﻦ ﺟﺮاﺣﻲ ﺑﻪﻋﻠﺖ ﻇﺮاﻓﺖ و
)ﭼﭗ ﻳﺎ راﺳﺖ( دارو ﺗﺰرﻳﻖ ﮔﺮدﻳﺪ و ﭘﺲ از اﻃﻤﻴﻨﺎن از اﺳﺘﻘﺮار ﺑﻠﻮك
ﺣﺴﺎﺳﻴﺖ ﺧﺎص ﺧﻮد ﻣﺪت زﻳﺎدﺗﺮي را ﺑﻪ ﺧﻮد اﺧﺘﺼﺎص ﺧﻮاﻫﺪ داد
ﺣﺴﻲ و ﺣﺮﻛﺘﻲ در اﻧﺪام ﺑﻌﺪ از ﭘﻨﺞ دﻗﻴﻘﻪ ﺑﻴﻤﺎر ﺑﻪﺣﺎﻟﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ
و در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﺑﺴﻴﺎري از اﻋﻤﺎل ﺟﺮاﺣﻲ ﻣﺸﺎﺑﻪ ﻧﻴﺎز ﺑﻪ ﺑﻲدردي و
ﭘﺸﺖ در ﻣﻲآﻣﺪ .ﭘﺲ از ﺑﺎز ﮔﺮداﻧﻴﺪن ﺑﻴﻤﺎر ﺑﻪﺣﺎﻟﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﺸﺖ
ﻣﺪت ﺑﻠﻮك ﺑﻴﺸﺘﺮي اﺳﺖ 8.ﻫﻴﭙﺮﺑﺎر ﺑﻮدن داروي ﺑﻲﺣﺴﻲ ﻣﻮﺿﻌﻲ ﺑﻪ
ﭘﺎي ﺳﻤﺖ ﻋﻤﻞ داراي ﺑﻠﻮك ﺣﺴﻲ و ﺣﺮﻛﺘﻲ ﺑﻴﺸﺘﺮي ﺑﻮد و ﺑﻪﻋﺒﺎرت
ﻣﺘﺨﺼﺺ ﺑﻴﻬﻮﺷﻲ اﺟﺎزه ﻣﻲدﻫﺪ ﻛﻪ ﻛﻨﺘﺮل ﺑﻴﺸﺘﺮي در ﻣﺤﻞ ﺗﻮزﻳﻊ
دﻳﮕﺮ ﭘﺎي ﻣﺤﻞ ﻋﻤﻞ ﺑﻪﻃﻮر ﻛﺎﻣﻞ ﺑﻠﻮك ﻣﻲﮔﺮدﻳﺪ و اﻳﻦ در ﺣﺎﻟﻲ ﺑﻮد
دارو داﺷﺘﻪ ﺑﺎﺷﺪ ،اﮔﺮ ﺑﻴﻤﺎران ﭘﺲ از اﻧﺠﺎم ﺑﻴﻬﻮﺷﻲ اﺳﭙﺎﻳﻨﺎل در
ﻛﻪ در زﻣﺎن آﻏﺎز ﻋﻤﻞ ﺟﺮاﺣﻲ ﭘﺎي دﻳﮕﺮ ﺑﻴﻤﺎران ﺗﻔﺎوت ﻓﺎﺣﺸﻲ از
وﺿﻌﻴﺖ ﺳﺮ ﺑﺎﻻ ﻗﺮار ﺑﮕﻴﺮﻧﺪ در ﺳﻄﺢ ﭘﺎﻳﻴﻦﺗﺮي از ﻧﺨﺎع ﺳﻄﺢ
ﻧﻈﺮ ﺑﻠﻮك ﺣﺴﻲ و ﺣﺮﻛﺘﻲ ﻧﺴﺒﺖ ﺑﻪ ﭘﺎي ﻣﻘﺎﺑﻞ داﺷﺖ .اﻃﻼﻋﺎت در
ﺑﻲﺣﺴﻲ ﻣﺴﺘﻘﺮ ﺷﺪه و ﻣﻴﺰان اﺛﺮ و ﻃﻮل ﻣﺪت ﺑﻲﺣﺴﻲ ﻧﻴﺰ ﺑﻴﺸﺘﺮ
ﻣﻮرد ﺳﻦ ،ﺟﻨﺴﻴﺖ ،ﻣﺪت ﻋﻤﻞ ﺟﺮاﺣﻲ ،ﻣﺪت ﺑﻠﻮك ﻋﺼﺒﻲ،
ﻣﻲﺷﻮد .اﮔﺮ ﺑﻴﻤﺎران ﭘﺲ از اﻧﺠﺎم ﺑﻴﻬﻮﺷﻲ اﺳﭙﺎﻳﻨﺎل ﺑﺎ ﻣﺤﻠﻮل ﻫﻴﭙﺮﺑﺎر
ﺑﻴﻤﺎريﻫﺎي ﻫﻤﺮاه ،ﻋﻠﺖ ﻋﻤﻞ ﺟﺮاﺣﻲ ،درﺻﺪ ﺗﻐﻴﻴﺮات ﻓﺸﺎر ﺧﻮن،
در وﺿﻌﻴﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﻗﺮار ﺑﮕﻴﺮﻧﺪ ﺳﻄﺢ ﺑﻲﺣﺴﻲ ﻣﻨﺎﺳﺐ در
ﺿﺮﺑﺎن ﻗﻠﺐ و ﺳﻄﺢ ﺑﻠﻮك ﻋﺼﺒﻲ ﺑﺮاي ﻛﻠﻴﻪ ﺑﻴﻤﺎران ﺛﺒﺖ ﮔﺮدﻳﺪ .در
ﺳﻤﺖ ﺟﺮاﺣﻲ ﺣﺎﺻﻞ ﺷﺪه ،ﺗﻐﻴﻴﺮات ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ ﻛﻢﺗﺮ ﺷﺪه و ﻃﻮل
ﻫﺮ دو ﮔﺮوه ﻗﺒﻞ از اﻗﺪام ﺑﻪ ﺑﻲﺣﺴﻲ ﻧﺨﺎﻋﻲ ﻓﺸﺎر ﺧﻮن و ﺿﺮﺑﺎن ﻗﻠﺐ
ﻣﺪت ﺑﻲﺣﺴﻲ ﻧﻴﺰ ﺑﻴﺸﺘﺮ ﻣﻲﺷﻮد .در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺑﻪ ﺑﺮرﺳﻲ ﺗﻐﻴﻴﺮات
ﺑﻴﻤﺎران ﭘﺲ از ﭘﻨﺞ دﻗﻴﻘﻪ از ﺧﻮاﺑﻴﺪن روي ﺗﺨﺖ اﺗﺎق ﻋﻤﻞ ﺛﺒﺖ و
ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ و ﻣﺪت ﺑﻲدردي در ﺑﻴﻤﺎران ﺗﺤﺖ ﺟﺮاﺣﻲ ﻋﺮوق اﻧﺪام
ﺑﻪﻋﻨﻮان ﻣﻴﺰان ﭘﺎﻳﻪ در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪ .ﺗﻤﺎﻣﻲ ﺑﻴﻤﺎران ﻳﻚ ﻣﻴﻠﻲﮔﺮم
ﺗﺤﺘﺎﻧﻲ ﺑﺎ دو روش ﺑﻲﺣﺴﻲ ﻧﺨﺎﻋﻲ در ﺣﺎﻟﺖﻫﺎي ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و
ﻣﻴﺪازوﻻم ورﻳﺪي ﺑﺮاي ﻛﺎﻫﺶ اﺿﻄﺮاب ﻣﻲﮔﺮﻓﺘﻨﺪ و ﺳﭙﺲ 5ml
ﻧﺸﺴﺘﻪ از ﺑﺎ اﺳﺘﻔﺎده از ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ %0/5ﻫﻴﭙﺮﺑﺎر ﭘﺮداﺧﺘﻴﻢ.
ﺑﻪازاي ﻫﺮ ﻛﻴﻠﻮﮔﺮم وزن ﺑﺪن ،از ﻣﺤﻠﻮل رﻳﻨﮕﺮ درﻳﺎﻓﺖ ﻣﻲﻧﻤﻮدﻧﺪ. ﻋﻼﻳﻢ ﺣﻴﺎﺗﻲ ﺑﻴﻤﺎران ﺷﺎﻣﻞ ﻓﺸﺎر ﺧﻮن ﺳﻴﺴﺘﻮﻟﻲ و دﻳﺎﺳﺘﻮﻟﻲ ،ﻓﺸﺎر
روش ﺑﺮرﺳﻲ
ﻣﺘﻮﺳﻂ ﺷﺮﻳﺎﻧﻲ و ﺿﺮﺑﺎن ﻗﻠﺐ ﺑﺎ دﺳﺘﮕﺎه ﻣﺎﻧﻴﺘﻮر اﻃﺎق ﻋﻤﻞ آرم
اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﻛﺎرآزﻣﺎﻳﻲ ﺑﺎﻟﻴﻨﻲ ﻣﻘﺎﻳﺴﻪاي ﺗﺼﺎدﻓﻲ
ﺳﻌﺎدت ) (Saadatﺳﺎﺧﺖ ﻛﺸﻮر اﻳﺮان ﺛﺒﺖ ﺷﺪ و در اداﻣﻪ اﻗﺪام ﺑﻪ
دوﺳﻮﻛﻮر ﻣﻲﺑﺎﺷﺪ ﻛﻪ در 40ﺑﻴﻤﺎر از ﻫﺮ دو ﮔﺮوه زن و ﻣﺮد و در
اﻧﺠﺎم ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ﺑﺎ ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ %0/5ﻫﻴﭙﺮﺑﺎر ﺷﺮﻛﺖ
(Merck,
ﺳﻨﻴﻦ 35-75ﺳﺎل ﻃﻲ ﻣﺪت ﻳﻚﺳﺎل ﺻﻮرت ﭘﺬﻳﺮﻓﺖ .ﻛﻠﻴﻪ ﺑﻴﻤﺎران
) Germanyﺑﻪﻣﻴﺰان 15ﻣﻴﻠﻲﮔﺮم ﮔﺮدﻳﺪ .ﭘﺲ از ﺗﺰرﻳﻖ داروي
ﻣﺒﺘﻼ ﺑﻪ ﻧﺎرﺳﺎﻳﻲ ﺧﻮنرﺳﺎﻧﻲ در اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺑﻮدﻧﺪ .در اﻳﻦ ﻣﻄﺎﻟﻌﻪ
ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ در دﻗﺎﻳﻖ ﻳﻚ ،ﺳﻪ ،ﭘﻨﺞ 25 ،20 ،15 ،10 ،و 30ﻓﺸﺎر ﺧﻮن
داروي اﻧﺘﺨﺎﺑﻲ ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ %0/5ﻫﻴﭙﺮﺑﺎر ﻛﻪ ﺑﻪﻋﻨﻮان ﻳﻚ داروي
ﺳﻴﺴﺘﻮﻟﻴﻚ ،دﻳﺎﺳﺘﻮﻟﻴﻚ ،ﻣﻴﺎﻧﮕﻴﻦ و ﺿﺮﺑﺎن ﻗﻠﺐ اﻧﺪازهﮔﻴﺮي و ﺛﺒﺖ
ﺑﻲﺣﺴﻲ ﻣﻮﺿﻌﻲ ﻃﻮﻻﻧﻲ اﺛﺮ ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﺳﺖ و ﺑﻪﺻﻮرت ﻣﻌﻤﻮل
ﻣﻲﺷﺪ .ﺟﻬﺖ ﺗﺼﺎدﻓﻲ ﻧﻤﻮدن ﻣﻄﺎﻟﻌﻪ از ﺟﻤﻊ دو ﻋﺪد ﺳﻤﺖ راﺳﺖ
ﻣﻲﺗﻮاﻧﺪ ﺑﻠﻮك ﻣﻮﺛﺮي را ﺑﻪﻣﺪت دو ﺳﺎﻋﺖ در ﻧﻮاﺣﻲ ﻣﻮرد ﻧﻴﺎز اﻳﻦ
ﺷﻤﺎره ﭘﺮوﻧﺪه ﺑﻴﻤﺎر اﺳﺘﻔﺎده ﻣﻲﺷﺪ .ﻋﺪد زوج در ﮔﺮوه ﻧﺸﺴﺘﻪ و ﻋﺪد
اﻋﻤﺎل ﺟﺮاﺣﻲ اﻳﺠﺎد ﻧﻤﺎﻳﺪ ﻣﻮرد اﺳﺘﻔﺎده ﻗﺮار ﮔﺮﻓﺖ .از ﻛﻠﻴﻪ ﺑﻴﻤﺎران
ﻓﺮد در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﻗﺮار ﻣﻲﮔﺮﻓﺘﻨﺪ .ﻳﻚ ﻧﻔﺮ از ﻫﻤﻜﺎران
ﻣﻮرد ﺑﺮرﺳﻲ رﺿﺎﻳﺖﻧﺎﻣﻪ ﻛﺘﺒﻲ اﺧﺬ ﺷﺪ و ﻃﺮح در ﻛﻤﻴﺘﻪ اﺧﻼق
ﻣﻄﺎﻟﻌﻪ ﺟﻬﺖ ﺛﺒﺖ ﻧﺘﺎﻳﺞ وارد اﻃﺎق ﻋﻤﻞ ﺷﺪه و ﭘﺮﺳﺶﻧﺎﻣﻪ ﺑﺮ اﺳﺎس
داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ﺑﻪ ﺗﺼﻮﻳﺐ رﺳﻴﺪ .در 40ﺑﻴﻤﺎر ﻛﻪ ﺑﻪ دو
ﻳﺎﻓﺘﻪﻫﺎي ﺑﺎﻟﻴﻨﻲ ﺛﺒﺖ ﻣﻲﮔﺮدﻳﺪ .ﺑﺮاي ﻳﻜﺴﺎنﺳﺎزي اﺟﺮاي ﻃﺮح ﺑﺴﺘﻪ
ﮔﺮوه 20ﻧﻔﺮه ﺗﻘﺴﻴﻢ ﺷﺪﻧﺪ در دو ﺣﺎﻟﺖ ﻧﺸﺴﺘﻪ و ﺣﺎﻟﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ
ﺑﻪ وﻇﺎﻳﻒ اﻓﺮاد ﻗﺒﻞ از اﺟﺮاي ﻃﺮح آﻣﻮزشﻫﺎي ﻻزم داده ﺷﺪ .ﺗﻤﺎﻣﻲ
ﭘﻬﻠﻮ داروي ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ﻫﻴﭙﺮﺑﺎرﻳﻚ ﺑﺎ ﻧﺎم ﺗﺠﺎري ﻣﺎرﻛﺎﻳﻴﻦ ﺷﺮﻛﺖ
ﺑﻴﻤﺎران ﺗﻮﺳﻂ ﻳﻚ ﻣﺘﺨﺼﺺ ﺑﻴﻬﻮﺷﻲ ﺗﺤﺖ ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ﻗﺮار
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
422
ﺗﻐﻴﻴﺮات ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ و ﻣﺪت ﺑﻲدردي در ﺑﻴﻤﺎران ﺗﺤﺖ ﺟﺮاﺣﻲ ﻋﺮوق اﻧﺪام ﺗﺤﺘﺎﻧﻲ
ﻣﻲﮔﺮﻓﺘﻨﺪ .ﺣﺠﻢ ﻣﺎﻳﻌﺎت ﻣﻮرد اﺳﺘﻔﺎده ،ﻃﻮل ﻣﺪت ﺑﻲﺣﺴﻲ در اﺗﺎق
داﺷﺘﻨﺪ ﻛﻪ در دو ﮔﺮوه ﻫﻤﺴﺎن ﺑﻮد ) .(P>0/05ﻣﺸﺨﺼﺎت دﻣﻮﮔﺮاﻓﻴﻚ
ﻋﻤﻞ و در زﻣﺎن اﻧﺘﻘﺎل ﺑﻪ رﻳﻜﺎوري و ﻣﺪت اﺳﺘﻘﺮار ﺑﻴﻤﺎران در
ﻛﻞ اﻓﺮاد در ﺟﺪول 1آﻣﺪه اﺳﺖ .اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري ﺑﻴﻦ
رﻳﻜﺎوري ﺗﺎ ﻗﺒﻞ از اﻧﺘﻘﺎل ﺑﻪ ﺑﺨﺶ ﺟﺮاﺣﻲ ،ﻧﻴﺎز ﺑﻪ اﺳﺘﻔﺎده از
ﺗﻐﻴﻴﺮات ﻓﺸﺎر ﺧﻮن ﻣﺘﻮﺳﻂ ﺷﺮﻳﺎﻧﻲ ،ﻓﺸﺎر ﺧﻮن دﻳﺎﺳﺘﻮﻟﻲ و ﻓﺸﺎر
وازوﭘﺮﺳﻮر ،ﺗﻮاﻧﺎﻳﻲ ﺣﺮﻛﺖ دادن اﻧﺪام ﺗﺤﺘﺎﻧﻲ و ﻋﻼﻳﻢ ﺣﻴﺎﺗﻲ ﺛﺒﺖ
ﺧﻮن ﺳﻴﺴﺘﻮﻟﻲ در ﻛﻠﻴﻪ زﻣﺎنﻫﺎي ﻣﻮرد ﺑﺮرﺳﻲ در دو ﮔﺮوه وﺟﻮد
ﻣﻲﮔﺮدﻳﺪ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺟﻬﺖ ﭘﮋوﻫﺶ ﺑﺮ روي
داﺷﺖ ) .(P=0/0001اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري ﺑﻴﻦ ﺗﻐﻴﻴﺮات ﺿﺮﺑﺎن
ﺑﻴﻤﺎران ﭘﺮﺧﻄﺮ در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪه ﺑﻮد ،ﻣﺤﺪودﻳﺖﻫﺎي ﻧﺴﺒﻲ و ﻣﻄﻠﻖ
ﻗﻠﺐ در ﻛﻠﻴﻪ زﻣﺎنﻫﺎي ﻣﻮرد ﺑﺮرﺳﻲ در دو ﮔﺮوه وﺟﻮد داﺷﺖ
و ﺑﻴﻤﺎراﻧﻲ ﻛﻪ
)(P=0/0001؛ اﻣﺎ در ﻣﻮرد ﺿﺮﺑﺎن ﻗﻠﺐ در دﻗﺎﻳﻖ ﻧﺨﺴﺖ و ﺳﻲام
ﺣﻴﻦ ﻋﻤﻞ ﺟﺮاﺣﻲ ﺗﻐﻴﻴﺮ روش ﺑﻴﻬﻮﺷﻲ از اﺳﭙﺎﻳﻨﺎل ﺑﻪ ﺑﻴﻬﻮﺷﻲ ﻋﻤﻮﻣﻲ
اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري را ﺑﻴﻦ دو ﮔﺮوه ﻧﺸﺎن ﻧﻤﻲداد ).(P>0/05
داﺷﺘﻨﺪ از ﻣﻄﺎﻟﻌﻪ ﺣﺬف ﮔﺮدﻳﺪﻧﺪ .ﻛﻨﺘﺮااﻧﺪﻳﻜﺎﺳﻴﻮنﻫﺎي اﺳﭙﺎﻳﻨﺎل ﺷﺎﻣﻞ
ﻣﻴﺰان ﻣﺎﻳﻊ ﻣﺼﺮﻓﻲ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺑﻪﻣﻴﺰان ﻣﻌﻨﻲداري ﺑﻴﺸﺘﺮ ﺑﻮد
ﻋﺪم رﺿﺎﻳﺖ ﺑﻴﻤﺎر ﺑﺮاي ﻫﻤﻜﺎري ،ﻋﻔﻮﻧﺖ ﭘﻮﺳﺘﻲ و زﻳﺮﺟﻠﺪي در
) 55 .(P=0/037درﺻﺪ از ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 10درﺻﺪ از ﮔﺮوه
ﻣﺤﻞ ورود ﺳﻮزن ،ﺳﺎﺑﻘﻪ ﺟﺮاﺣﻲ ﻧﺨﺎع و ﺳﺘﻮن ﻓﻘﺮات در ﻣﺤﻞ ورود
ﻧﺸﺴﺘﻪ ﺗﻮاﻧﺎﻳﻲ ﺣﺮﻛﺖ ﻳﻚ ﭘﺎيﺷﺎن را ﭘﺲ از ﭘﻨﺞ دﻗﻴﻘﻪ از ﺷﺮوع
ﺳﻮزن و دﻓﻮرﻣﻴﺘﻲ ﺳﺘﻮن ﻓﻘﺮات ﺑﻮدﻧﺪ .در ﻧﻬﺎﻳﺖ آﻧﺎﻟﻴﺰ آﻣﺎري ﺑﺎ ﻛﻤﻚ
ﺑﻲﺣﺴﻲ داﺷﺘﻨﺪ ﻛﻪ اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري را ﻧﺸﺎن ﻣﻲداد
ﻧﺮماﻓﺰار SPSSوﻳﺮاﺳﺖ 16اﻧﺠﺎم ﺷﺪ و آزﻣﻮن ﻣﻮرد اﺳﺘﻔﺎده در ﻣﻮرد
) .(P<0/05ﺻﻔﺮ درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 20درﺻﺪ در
Kolmogorov-
ﮔﺮوه ﻧﺸﺴﺘﻪ ﻣﺼﺮف وازوﭘﺮﺳﻮر داﺷﺘﻨﺪ ﻛﻪ اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري
Student’s t-test ،Smirnov testﺑﻮد و در ﻣﻮرد ﻣﺘﻐﻴﺮﻫﺎي ﻛﻴﻔﻲ ﻧﻴﺰ از
را ﻧﺸﺎن ﻣﻲداد ) .(P=0/034ﺷﺮوع ﺑﻲﺣﺴﻲ در دو ﮔﺮوه اﺧﺘﻼف
و Fisher’s exact testاﺳﺘﻔﺎده ﮔﺮدﻳﺪ .ﺳﻄﺢ ﻣﻌﻨﻲدار
آﻣﺎري ﻣﻌﻨﻲداري ﻧﺪاﺷﺖ ) ،(P>0/05اﻣﺎ ﻃﻮل ﻣﺪت ﺑﻲﺣﺴﻲ در ﮔﺮوه
ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ،ﺑﺎﻻﺗﺮ رﻓﺘﻦ ﺳﻄﺢ ﺑﻲﺣﺴﻲ از
T10
ﻣﻘﺎﻳﺴﻪ ﻣﺘﻐﻴﺮﻫﺎي ﻛﻤﻲ در دو ﮔﺮوه ﺑﺮ اﺳﺎس ﻧﺘﺎﻳﺞ آزﻣﻮنﻫﺎي
2
ﺑﺎ اﻧﺤﺮافﻣﻌﻴﺎر %0/05در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪ.
ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﺑﻪﻣﻴﺰان ﻣﻌﻨﻲداري ﻃﻮﻻﻧﻲﺗﺮ ﺑﻮده و ﺗﺎ زﻣﺎن اﻧﺘﻘﺎل ﺑﻴﻤﺎران ﺑﻪ رﻳﻜﺎوري اﻧﺪازهﮔﻴﺮي ﮔﺮدﻳﺪ در ﺑﻴﻤﺎران ﻧﺸﺴﺘﻪ درد در
ﻳﺎﻓﺘﻪﻫﺎ
رﻳﻜﺎوري ﺑﻪﻋﻠﺖ ﺑﺎزﮔﺸﺖ ﺣﺲ ﻣﺤﻞ ﻋﻤﻞ ﺟﺮاﺣﻲ زودﺗﺮ آﻏﺎز
ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ 52ﺳﺎل و در ﮔﺮوه ﻧﺸﺴﺘﻪ
ﮔﺮدﻳﺪ ،در ﻳﻚ ﺳﺎﻋﺖ اول ﭘﺲ از ورود ﺑﻪ رﻳﻜﺎوري ﻣﺼﺮف ﻣﺴﻜﻦ
56/1ﺳﺎل ﺑﻮد ﻛﻪ در دو ﮔﺮوه ﻫﻤﺴﺎن ﺑﻮد ) 90 .(P>0/05درﺻﺪ در
دﻳﺪه ﺷﺪ ﻛﻪ اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري را ﻧﺸﺎن ﻣﻲداد .اﻳﻦ اﺧﺘﻼف
ﻫﺮ دو ﮔﺮوه ﻣﺬﻛﺮ ﺑﻮدﻧﺪ ) 95 .(P>0/05درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ
75درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ در 10درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ
ﭘﻬﻠﻮ و 85درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺳﻴﮕﺎر ﻣﻲﻛﺸﻴﺪﻧﺪ ﻛﻪ در دو ﮔﺮوه
اﻧﺪازهﮔﻴﺮي و ﺛﺒﺖ ﮔﺮدﻳـﺪ ) .(P=0/0001در ﭘﻨﺞ درﺻﺪ ﮔﺮوه ﺧﻮاﺑﻴﺪه
ﻫﻤﺴﺎن ﺑﻮد ) 60 .(P>0/05درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 55 درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﻣﻮاد ﻣﺨﺪر ﻣﺼﺮف ﻣﻲﻧﻤﻮدﻧﺪ )15 ،(P>0/05 درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 15درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ اﻟﻜﻞ
ﺟﺪول :1-ﻣﺸﺨﺼﺎت دﻣﻮﮔﺮاﻓﻴﻚ ﻛﻞ اﻓﺮاد ﻣﻮرد ﺑﺮرﺳﻲ ﻓﺮاواﻧﻲ
درﺻﺪ ﻓﺮاواﻧﻲ
ﺟﻨﺲ ﻣﺬﻛﺮ
36
90
اﺳﺘﻌﻤﺎل ﺳﻴﮕﺎر
36
90
درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 25درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺳﺎﺑﻘﻪ
ﻣﺼﺮف ﻣﻮاد ﻣﺨﺪر
23
57/5
اﻧﻔﺎرﻛﺘﻮس ﻣﻴﻮﻛﺎرد داﺷﺘﻨﺪ ) 45 ،(P>0/05درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ
ﻣﺼﺮف اﻟﻜﻞ
6
15
ﭘﻬﻠﻮ و 65درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺳﺎﺑﻘﻪ دﻳﺎﺑﺖ داﺷﺘﻨﺪ )30 ،(P>0/05
ﺳﺎﺑﻘﻪ اﻧﻔﺎرﻛﺘﻮس ﻣﻴﻮﻛﺎرد
8
20
درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 65درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺳﺎﺑﻘﻪ
ﺳﺎﺑﻘﻪ دﻳﺎﺑﺖ
22
55
ﺑﻴﻤﺎري اﻳﺴﻜﻤﻴﻚ ﻗﻠﺒﻲ داﺷﺘﻨﺪ ) (P>0/05و ﺑﺎﻻﺧﺮه 40درﺻﺪ در
ﺳﺎﺑﻘﻪ ﻫﻴﭙﺮﺗﺎﻧﺴﻴﻮن
20
50
ﺳﺎﺑﻘﻪ ﺑﻴﻤﺎري اﻳﺴﻜﻤﻴﻚ ﻗﻠﺒﻲ
19
47/5
ﻣﺼﺮف ﻣﻲﻛﺮدﻧﺪ ) 40 ،(P>0/05درﺻﺪ در ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 60درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺳﺎﺑﻘﻪ ﺑﻴﻬﻮﺷﻲ ﻧﺪاﺷﺘﻨﺪ )15 ،(P>0/05
ﮔﺮوه ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ و 60درﺻﺪ در ﮔﺮوه ﻧﺸﺴﺘﻪ ﺳﺎﺑﻘﻪ ﻫﻴﭙﺮﺗﺎﻧﺴﻴﻮن
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻣﺸﺨﺼﻪ
ﻣﺤﻤﺪرﺿﺎ ﻣﻬﺎﺟﺮ و ﻫﻤﻜﺎران
ﺟﺪول :2-ﻛﻠﻴﻪ ﻧﺘﺎﻳﺞ ﺑﻪدﺳﺖ آﻣﺪه در دو ﮔﺮوه ﻣﻮرد ﺑﺮرﺳﻲ ﮔﺮوه MAPC1ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC2ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC3ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC4ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC5ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC6ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC7ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ MAPC8ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC1ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC2ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC3ﭘﻮرﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC4ﭘﻮرﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC5ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC6ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC7ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SBPC8ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ
ﻣﻴﺎﻧﮕﻴﻦ 0/8500 -6/6000 -5/7600 -12/2000 -8/3000 -14/7000 -8/0500 -12/4500 -7/9500 -12/4500 -7/3500 -11/6000 -6/8000 -11/35000 -6/5000 -11/3500 -0/5000 -6/4000 -6/2000 -10/9000 -8/9500 -12/6500 -8/7000 -11/9000 -8/5500 -11/1500 -7/9500 -11/0500 -7/9000 -11/0500 -7/5500 -10/6500
423
اداﻣﻪ ﺟﺪول :2-ﻛﻠﻴﻪ ﻧﺘﺎﻳﺞ ﺑﻪدﺳﺖ آﻣﺪه در دو ﮔﺮوه ﻣﻮرد ﺑﺮرﺳﻲ اﻧﺤﺮافﻣﻌﻴﺎر 0/1273 3/10178 2/19749 4/40813 2/67739 6/44999 2/51850 5/18576 3/51650 4/43045 2/60111 4/04449 2/14231 3/50188 1/87785 2/72223 1/46898 2/72223 2/26181 4/14094 3/10305 4/53379 3/24605 3/52286 2/87411 3/34467 2/64525 3/70313 2/78908 3/03445 2/45867 3/01357
ﮔﺮوه DBPC1ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC2ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC3ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC4ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC5ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC6ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC7ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ DBPC8ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC1ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ SHRC2ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC3ﭘﻮرﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC4ﭘﻮرﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC5ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC6ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC7ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ HRC8ﭘﻮزﻳﺸﻦ ﻟﺘﺮال ﻧﺸﺴﺘﻪ
ﻣﻴﺎﻧﮕﻴﻦ -0/9500 -6/1000 -5/5500 -9/3000 -7/4000 -9/5500 -7/6600 -9/7500 -7/2500 -9/0500 -6/7000 -9/2000 -6/3000 -9/0500 -6/3000 -8/6500 4/1500 4/5000 3/7500 7/3000 3/7000 10/2500 3/4000 9/7500 3/0500 9/1500 3/4500 7/4500 2/8500 6/3000 2/7500 4/8500
اﻧﺤﺮافﻣﻌﻴﺎر 0/94451 2/67346 2/41650 3/19704 2/77963 4/08431 2/68475 2/53138 2/67296 2/48088 2/40832 2/50473 2/67739 2/54383 2/40822 2/47673 1/08942 4/01989 1/25132 3/62883 0/97672 6/80997 1/78885 6/7704 1/43179 6/20400 1/70062 6/79905 2/10950 6/36166 1/88833 5/49946
ﺑﻪ ﭘﻬﻠﻮ و 30درﺻﺪ ﮔـﺮوه ﻧﺸـﺴﺘﻪ ،ﺗﻬـﻮع و اﺳـﺘﻔﺮاغ دﻳـﺪه ﺷـﺪ ﻛـﻪ
ﺑﻬﺒﻮد ﻣﻲﺑﺨﺸﺪ 6.اﻳﻦ ﺑﻴﻤﺎران ﺑﻪﻃﻮر ﻋﻤﺪه در ﺳﻨﻴﻦ ﻣﻴﺎنﺳـﺎل و ﻣـﺴﻦ
اﺧﺘﻼف آﻣﺎري ﻣﻌﻨﻲداري را ﻧﺸﺎن ﻧﻤﻲداد )) (P>0/05ﺟﺪول .(2
ﺑﻮده و ﻣﺸﻜﻼﺗﻲ ﻣﺎﻧﻨﺪ ﺑﺮوﻧﺸﻴﺖ ،ﺑﻴﻤﺎريﻫﺎي اﻧﺴﺪادي رﻳﻮي ،دﻳﺎﺑﺖ، ﺑﻴﻤﺎريﻫﺎي ﻋﺮوﻗﻲ ﻣﺎﻧﻨﺪ ﺑﻮرﮔﺮ را ﺑﻪﻫﻤﺮاه ﺧﻮد دارﻧﺪ 7.از ﻃﺮف دﻳﮕﺮ
ﺑﺤﺚ ﺑﻪﻋﻠﺖ ﺑﻠﻮك ﻧﺎﺣﻴﻪاي در اﻧـﺪام ﺗﺤﺘـﺎﻧﻲ ﺗﻨﻬـﺎ ﺳﻴـﺴﺘﻢ ﻋـﺼﺒﻲ ﺣـﺴﻲ
اﻳﻦ ﺟﺮاﺣﻲ ﺑﻪﻋﻠﺖ ﻇﺮاﻓﺖ و ﺣﺴﺎﺳﻴﺖ ﺧﺎص ﺧﻮد ﻣﺪت زﻳﺎدﺗﺮي را ﺑﻪ ﺧـﻮد اﺧﺘـﺼﺎص ﺧﻮاﻫـﺪ داد و در ﻣﻘﺎﻳـﺴﻪ ﺑـﺎ ﺑـﺴﻴﺎري از اﻋﻤـﺎل 8
ﺣﺮﻛﺘﻲ را ﺑﻠﻮك ﻧﻤﻮده و ﺑﺎ ﻛﺎﻫﺶ واﺿﺢ در ﺗﻮﻧﻴﺴﻴﺘﻪ ﻋﺮوﻗﻲ ﻣﻲﺗﻮاﻧﺪ
ﺟﺮاﺣﻲ ﻣﺸﺎﺑﻪ ﻧﻴﺎز ﺑﻪ ﺑﻲدردي و ﻣﺪت ﺑﻠﻮك ﺑﻴﺸﺘﺮي اﺳـﺖ .در اﻳـﻦ
ﺧﻮنرﺳﺎﻧﻲ اﻧﺪام ﺗﺤﺘﺎﻧﻲ را ﺑﻪﻃﻮر ﻣﻮﺛﺮي ﺑﻬﺒﻮد ﺑﺨﺸﺪ ،از ﻃﺮف دﻳﮕﺮ
ﻣﻄﺎﻟﻌﻪ داروي اﻧﺘﺨﺎﺑﻲ ﺑﻮﭘﻴﻮاﻛـﺎﻳﻴﻦ %0/5ﻫﻴﭙﺮﺑـﺎر ﻛـﻪ ﺑـﻪﻋﻨـﻮان ﻳـﻚ
ﻛﻢﺗﺮﻳﻦ اﺛﺮ ﻣﺴﺘﻘﻴﻢ را ﺑﺮ روي ﻗﻠـﺐ رﻳـﻪ و ﻣﻐـﺰ داﺷـﺘﻪ و ﺑـﺎ ﻛـﺎﻫﺶ
داروي ﻃﻮﻻﻧﻲ اﺛﺮ ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﺳﺖ و ﺑﻪﺻـﻮرت ﻣﻌﻤـﻮل ﻣـﻲﺗﻮاﻧـﺪ
ﻣﻘﺎوﻣﺖ ﺑﺮ ﺳﺮ راه ﺑﺮونده ﻗـﻠﺒﻲ ﻗﺪرت ﭘﻤـﭗ و اﻧـﺪﻛﺲ ﻗﻠﺒﻲ را ﻧﻴـﺰ
ﺑﻠﻮك ﻣﻮﺛﺮي را ﺑﻪﻣﺪت دو ﺳﺎﻋﺖ در ﻧﻮاﺣﻲ ﻣـﻮرد ﻧﻴـﺎز اﻳـﻦ اﻋﻤـﺎل
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﺗﺤﺖ ﺟﺮاﺣﻲ ﻋﺮوق اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺑﻴﻤﺎرانM.R. دردي در Mohajer et ﺑﻲ al.ﺗﻐﻴﻴﺮات ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ و ﻣﺪت
424
در اﻧﮕﻠـﻴﺲ اﻧﺠـﺎم ﺷـﺪ ﺑـﺮChadwick در ﻣﻄﺎﻟﻌﻪاي ﻛﻪ ﺗﻮﺳﻂ.ﮔﺮدد
ﺑﻴﻤﺎر ﻛﻪ ﺑـﻪ دو40 در9.ﺟﺮاﺣﻲ اﻳﺠﺎد ﻧﻤﺎﻳﺪ ﻣﻮرد اﺳﺘﻔﺎده ﻗﺮار ﮔﺮﻓﺖ
ﺧﻼف ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﺑﻪ اﻳﻦ ﻧﺘﻴﺠﻪ رﺳﻴﺪ ﻛﻪ ﺑﻴﻦ وﺿﻌﻴﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠـﻮ
ﻧﻔﺮه ﺗﻘﺴﻴﻢﺑﻨﺪي ﺷﺪﻧﺪ در دو ﺣﺎﻟﺖ ﻧﺸﺴﺘﻪ و ﺣﺎﻟﺖ ﺧﻮاﺑﻴﺪه20 ﮔﺮوه
اﺧﺘﻼﻓﻲ از ﻧﻈﺮ ﻧﺘﺎﻳﺞ ﺑﻪدﺳﺖ آﻣﺪه از ﻧﻈﺮ وﺿﻌﻴﺖ،و وﺿﻌﻴﺖ ﻧﺸﺴﺘﻪ
ﺗﺰرﻳـﻖ3ml ﺑـﻪﻣﻴـﺰان%0/5 ﺑﻪ ﭘﻬﻠـﻮ داروي ﺑﻮﭘﻴﻮاﻛـﺎﻳﻴﻦ ﻫﻴﭙﺮﺑﺎرﻳـﻚ
ﻫﻤﺎﻧﻨـﺪ، در آﻣﺮﻳﻜـﺎEmerson ﻣﻄﺎﻟﻌـﻪ16.ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ وﺟـﻮد ﻧـﺪارد
در ﮔـﺮوه. در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪT10 ﮔﺮدﻳﺪه و ﺳﻄﺢ ﺑﻲﺣﺴﻲ ﺑﻴﻤﺎران در
ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﺑﻪ اﻳﻦ ﻧﺘﻴﺠﻪ رﺳﻴﺪ ﻛـﻪ ﺑـﻴﻦ وﺿـﻌﻴﺖ ﺧﻮاﺑﻴـﺪه ﺑـﻪ ﭘﻬﻠـﻮ و
ﺧﻮاﺑﺎﻧـﺪه25 ﻧﺸﺴﺘﻪ ﺑﻴﻤﺎران ﭘﺲ از اﻧﺠﺎم ﺗﻜﻨﻴﻚ ﺑـﺎ ﺳـﻮزن اﺳـﭙﺎﻳﻨﺎل
وﺿــﻌﻴﺖ ﻧﺸــﺴﺘﻪ اﺧــﺘﻼف آﻣــﺎري ﻣﻌﻨ ـﻲداري وﺟــﻮد دارد و ﻣﻴــﺰان
در.ﺷﺪه و ﭘﺲ از اﺳﺘﻘﺮار ﺑﻠﻮك اﺟﺎزه آﻏـﺎز ﻋﻤـﻞ ﺟﺮاﺣـﻲ داده ﺷـﺪ
De
17
در ﻣﻄﺎﻟﻌﻪ.ﺗﻐﻴﻴﺮات در ﭘﻮزﻳﺸﻦ ﺧﻮاﺑﻴﺪه ﻛﻢﺗﺮ از ﻧﺸﺴﺘﻪ ﻣﻲﺑﺎﺷﺪ
ﺑﻴﻤﺎران ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﻬﻠﻮ ﻧﻴﺰ ﭘﺲ از ﺧﻮاﺑﺎﻧﻴﺪن ﺑﻴﻤﺎران ﺑـﻪﺳـﻤﺖ ﻣـﻮرد
در ﻫﻠﻨﺪ ﻧﻴﺰ اﺧﺘﻼﻓﻲ ﺑﻴﻦ ﺗﻐﻴﻴﺮات ﻫﻤﻮدﻳﻨﺎﻣﻴﻚ ﺑﻴﻦ دو ﭘﻮزﻳـﺸﻦLaat
ﻋﻤﻞ )ﭼﭗ ﻳﺎ راﺳﺖ( داروي ﻣﺬﻛﻮر ﺗﺰرﻳـﻖ ﮔﺮدﻳـﺪ و ﺑـﻪﻣـﺪت ﭘـﻨﺞ
در ﻣﺠﻤﻮع ﺑﺮ اﺳـﺎس ﻧﺘـﺎﻳﺞ ﺣﺎﺻـﻞ از18.ﺧﻮاﺑﻴﺪه و ﻧﺸﺴﺘﻪ ﭘﻴﺪا ﻧﺸﺪ
ﮔﺮوه دوم ﭘﺲ از ﺑـﺎز.دﻗﻴﻘﻪ ﺑﻴﻤﺎران در اﻳﻦ ﻣﻮﻗﻌﻴﺖ ﺣﻔﻆ ﻣﻲﮔﺮدﻳﺪﻧﺪ
اﻳﻦ ﻣﻄﺎﻟﻌﻪ و ﻣﻘﺎﻳﺴﻪ آنﻫﺎ ﺑﺎ ﺳﺎﻳﺮ ﻣﻄﺎﻟﻌﺎت اﻧﺠﺎم ﺷﺪه در اﻳـﻦ زﻣﻴﻨـﻪ
ﮔﺮداﻧﻴﺪن ﺑﻪﺣﺎﻟﺖ ﺧﻮاﺑﻴﺪه ﺑﻪ ﭘﺸﺖ در ﭘﺎي ﻣﺬﻛﻮر در ﺳﻤﺖ ﺧﻮاﺑﻴـﺪن
ﭼﻨﻴﻦ اﺳﺘﻨﺒﺎط ﻣﻲﺷـﻮد ﻛـﻪ ﻣﻴـﺰان ﺗﻐﻴﻴـﺮات در ﺑﻴﻬﻮﺷـﻲ اﺳـﭙﺎﻳﻨﺎل در
ﺑﻴﻤﺎر داراي ﺑﻠﻮك ﻋﻤﻴﻖﺗﺮي ﺑﻮده و ﺑﻪﻋﺒﺎرت دﻳﮕﺮ ﭘـﺎي ﻣﺤـﻞ ﻋﻤـﻞ
ﭘﻮزﻳﺸﻦ ﺧﻮاﺑﻴﺪه ﻛﻢﺗﺮ از ﻧﺸﺴﺘﻪ ﻣﻲﺑﺎﺷـﺪ و ﻟـﺬا اﺳـﺘﻔﺎده از ﭘﻮزﻳـﺸﻦ
اﻳﻦ در ﺣـﺎﻟﻲ اﺳـﺖ ﻛـﻪ در زﻣـﺎن آﻏـﺎز.ﺑﻪﻃﻮر ﻛﺎﻣﻞ ﺑﻠﻮك ﻣﻲﮔﺮدﻳﺪ
ﺧﻮاﺑﻴﺪه ﺑﺮاي ﺑﻴﻬﻮﺷﻲﻫﺎي اﺳﭙﺎﻳﻨﺎل در اﻓﺮاد ﺗﺤﺖ ﺟﺮاﺣﻲﻫﺎي ﻋـﺮوق
ﻋﻤﻞ ﺟﺮاﺣﻲ ﭘﺎي دﻳﮕﺮ ﺑﻴﻤﺎران ﺗﻔﺎوت ﻓﺎﺣﺶ و ﻛﻢﺗﺮي از ﻧﻈﺮ ﺑﻠﻮك
اﻧﺪام ﺗﺤﺘﺎﻧﻲ و ﺳﺎﻳﺮ ﺟﺮاﺣﻲﻫﺎﻳﻲ ﻛﻪ ﺗﻐﻴﻴـﺮات ﻫﻤﻮدﻳﻨﺎﻣﻴـﻚ زﻳـﺎد در
اﻳﻦ ﺑﻠﻮك ﻋﺼﺒﻲ ﻣﻨﺠﺮ ﺑﻪ.ﺣﺴﻲ و ﺣﺮﻛﺘﻲ ﻧﺴﺒﺖ ﺑﻪ ﭘﺎي ﻣﻘﺎﺑﻞ داﺷﺖ
در اﻧﺘﻬـﺎ ﭘﻴـﺸﻨﻬﺎد ﻣـﻲﺷـﻮد. ﺗﻮﺻـﻴﻪ ﻣـﻲﺷـﻮد،آنﻫﺎ ﺧﻄﺮﻧﺎك اﺳـﺖ
اﻳﻦ ﺷﺪ ﻛـﻪ ﻣﺰاﻳـﺎ و ﻣﻌﺎﻳـﺐ اﻳـﻦ دو روش ﺑﺮرﺳـﻲ و ﻃـﻲ ﺟـﺪوﻟﻲ
.ﻣﻄﺎﻟﻌﺎت ﺑﻴﺸﺘﺮي ﺑﻪﻣﻨﻈﻮر ﺗﺄﻳﻴﺪ ﻳﺎﻓﺘﻪﻫﺎي اﻳﻦ ﻣﻄﺎﻟﻌﻪ اﻧﺠﺎم ﺷﻮد
ﺑﻪﺻﻮرت ﻣﺘﻐﻴﺮﻫﺎي اﻧﺪازهﮔﻴﺮي ﺷﺪه ﺑﻪﺻﻮرت ﻧﺘﺎﻳﺞ اﻳﻦ ﻣﻄﺎﻟﻌﻪ اﻋﻼم
References 1. Norris EJ. Anesthesia for vascular surgery. In: Miller RD, editor. Miller's Anesthesia. 5th ed. Philadelphia: Churchill Livingston; Vol. 2. 2005. p. 2051-125. 2. Singh N, Sidawy AN, Dezee K, Neville RF, Weiswasser J, Arora S, et al. The effects of the type of anesthesia on outcomes of lower extremity infrainguinal bypass. J Vasc Surg 2006;44(5):964-8; discussion 968-70. 3. Mangano DT. Perioperative cardiac morbidity. Anesthesiology 1990;72(1):153-84. 4. Hertzer NR. Cardiac risk factors in peripheral vascular surgery. In: Estafanous FG, editor. Anesthesia and the Heart Patient. Oxford: Buterworth Heineman; 1989. p. 173-95. 5. Tisi GM. Preoperative evaluation of pulmonary function. Validity, indications, and benefits. Am Rev Respir Dis 1979;119(2):293-310. 6. Christopherson R, Beattie C, Frank SM, Norris EJ, Meinert CL, Gottlieb SO, et al. Perioperative morbidity in patients randomized to epidural or general anesthesia for lower extremity vascular surgery. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology 1993;79(3):422-34. 7. Mackay CA, Razik W, Simms MH. Local anaesthetic for lowerlimb revascularization in high-risk patients. Br J Surg 1997;84(8):1096-8. 8. Slogoff S, Keats AS. Does perioperative myocardial ischemia lead to postoperative myocardial infarction? Anesthesiology 1985;62(2):107-14. 9. Rosenfeld BA, Beattie C, Christopherson R, Norris EJ, Frank SM, Breslow MJ, et al. The effects of different anesthetic regimens on fibrinolysis and the development of postoperative arterial thrombosis. Perioperative Ischemia Randomized Anesthesia Trial Study Group. Anesthesiology 1993;79(3):435-43.
10. Norris EJ, Beattie C, Perler BA, Martinez EA, Meinert CL, Anderson GF, et al. Double-masked randomized trial comparing alternate combinations of intraoperative anesthesia and postoperative analgesia in abdominal aortic surgery. Anesthesiology 2001;95(5):1054-67. 11. Horlocker TT, Heit JA. Low molecular weight heparin: biochemistry, pharmacology, perioperative prophylaxis regimens, and guidelines for regional anesthetic management. Anesth Analg 1997;85(4):874-85. 12. Urmey WF, Rowlingson J. Do antiplatelet agents contribute to the development of perioperative spinal hematoma? Reg Anesth Pain Med 1998;23(6 Suppl 2):146-51. 13. Guinard JP, Mulroy MF, Carpenter RL. Aging reduces the reliability of epidural epinephrine test doses. Reg Anesth 1995;20(3):193-8. 14. Kooger Infante NE, Van Gessel E, Forster A, Gamulin Z. Extent of hyperbaric spinal anesthesia influences the duration of spinal block. Anesthesiology 2000;92(5):1319-23. 15. Chohan U, Afshan G, Hoda MQ, Mahmud S. Haemodynamic effects of unilateral spinal anesthesia in high risk patients. J Pak Med Assoc 2002;52(2):66-9. 16. Chadwick IS, Eddleston JM, Chandelier CK, Pollard BJ. Haemodynamic effects of the position chosen for the insertion of an epidural catheter. Int J Obstet Anesth 1993;2(4):197-201. 17. Emerson RJ, Banasik JL. Effect of position on selected hemodynamic parameters in postoperative cardiac surgery patients. Am J Crit Care 1994;3(4):289-99. 18. de Laat E, Schoonhoven L, Grypdonck M, Verbeek A, de Graaf R, Pickkers P, van Achterberg T. Early postoperative 30 degrees lateral positioning after coronary artery surgery: influence on cardiac output. J Clin Nurs 2007;16(4):654-61.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
Tehran University Medical Journal;ﻫﻤﻜﺎران Vol. 69, وNo. 7, October 2011: 420-425
100
The comparison between lateral spinal anesthesia and sitting positions in lower limb vascular surgery
Abstract Mohammad Reza Mohajer M.D.1 Kasra Karvandian M.D.1* Zahid Hussain Khan M.D.1 Afshin Jafarzadeh M.D.1 Soheila Dabiran M.D.2 1- Department of Anesthesiology and Critical Care, Tehran University of Medical Sciences, Tehran, Iran. 2- Department of Community Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Received: May 04, 2011 Accepted: July 04, 2011
Background: Patients who require surgery on the lower extremities are considered to be a high risk group from the point of anesthesia. This study was performed to compare sitting and lateral positions in spinal anesthesia method with hyperbaric bupivacaine 0.5% for hemodynamic status and analgesic period in patients under vascular surgery of
the lower limbs in Imam-Khomeini Hospital Complex affiliated to Tehran University of Medical Sciences in 2009. Methods: In this study 40 patients were divided into two groups of 20 to undergo spinal anesthesia with 3 ml of hyperbaric bupivacaine 0.5% injected into the subarachnoid space in sitting or lateral positions. The anesthesia was performed at T10 level and the hemodynamic status and analgesic periods were compared in the two groups. Results: The changes in mean arterial blood pressure and systolic and diastolic blood pressures were different between the two groups (P<0.05). Except in the first and thirtieth minutes, the changes in heart rate (HR) were significantly different throughout the study between the two groups (P<0.04) and they were higher in sitting position. The duration of analgesia was significantly longer in lateral position (P<0.04) and the use of fluid was significantly larger in the sitting group (P<0.05). Conclusion: According to the obtained results, the changes in hemodynamic variables were significantly lower in the group in lateral versus sitting position in patients undergoing spinal anesthesia with bupivacaine for vascular surgery of the lower limb. Keywords: Bupivacaine, position, spinal anesthesia, vascular surgery.
*
Corresponding author: Keshavarz Blvd., Imam Khomeini Hospital, Tehran, Iran. Tel: +98-21-88249920 E-mail: kassramail@yahoo.com
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
ﻛﺮده426-431 ،1390 زﻧﺎنﻣﻬﺮ ﺷﻤﺎره ،7 دوره ، 69 ﺗﻬﺮان، ﻋﻠﻮمﺑﺮﭘﺰﺷﻜ داﻧﺸﮕﺎه ﻳﻚﭘﺰﺷﻜ ﺗﺄﺛﻴﺮﻜﺪه ﻣﺠﻠﻪ داﻧﺸ ﺗﻤﺮﻳﻦ ﻟﻨﻔﻮﺳﻴﺖ در اﺑﺴﺘﺎﺗﻴﻦ ﺑﻴﺎنﻲژن ﻫﻮازي ﺟﻠﺴﻪﻲ،ﺗﻤﺮﻳﻦ
ﺗﺄﺛﻴﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ در زﻧﺎن ﺗﻤﺮﻳﻦ ﻛﺮده
ﭼﻜﻴﺪه
*1
اﻣﻴﺮ رﺷﻴﺪﻟﻤﻴﺮ
ﻣﻬﺪﻳﻪ اﺑﺮاﻫﻴﻢﻧﻴﺎ
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1390/02/14 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/05/24 :
زﻣﻴﻨﻪ و ﻫﺪف :اﺑﺴﺘﺎﺗﻴﻦ ،ﻳﻚ ﭘﭙﺘﻴﺪ ﺿﺪ اﺷﺘﻬﺎ اﺳﺖ .ﻣﻄﺎﻟﻌﺎت ﻧﺸﺎن ﻣﻲدﻫﺪ ﻛﻪ اﺑﺴﺘﺎﺗﻴﻦ در ﺗﻌﺎدل اﻧﺮژي ،ﺗﺮﺷﺢ
1 2
ﻋﻠﻲ اﻛﺒﺮ ﻫﺎﺷﻤﻲ ﺟﻮاﻫﺮي
ﻫﻮرﻣﻮن رﺷﺪ
)(GH
و ﺗﻐﻴﻴﺮات وزن ﺑﺪن ﻧﻘﺶ دارد و ﻣﺸﺨﺺ ﺷﺪه ﻛﻪ از ﻧﻈﺮ ﻓﻴﺰﻳﻮﻟﻮژﻳﻜﻲ ﻋﻤﻠﻜﺮد ﻣﺘﻀﺎدي ﺑﺎ
ﮔﺮﻟﻴﻦ دارد .ﻫﺪف از ﺗﺤﻘﻴﻖ ﺣﺎﺿﺮ ﺑﺮرﺳﻲ اﺛﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ) 1/5ﻣﺎﻳﻞ دوﻳﺪن( ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ -1ﮔﺮوه ﻓﻴﺰﻳﻮﻟﻮژي ورزﺷﻲ
ﻟﻨﻔﻮﺳﻴﺖﻫﺎي زﻧﺎن ﺗﻤﺮﻳﻦﻛﺮده ﻣﻲﺑﺎﺷﺪ .روش ﺑﺮرﺳﻲ :ﺗﻌﺪاد 16زن ﺗﻤﺮﻳﻦﻛﺮده ﺧﺮاﺳﺎﻧﻲ ﭘﺲ از ﻓﺮاﺧﻮان اﻧﺘﺨﺎب و
-2ﮔﺮوه درﻣﺎﻧﮕﺮي ورزﺷﻲ
ﺑﻪﻃﻮر ﺗﺼﺎدﻓﻲ ﺑﻪ دو ﮔﺮوه ﻛﻨﺘﺮل و ﺗﺠﺮﺑﻲ ﺗﻘﺴﻴﻢ ﺷﺪﻧﺪ .ﮔﺮوه ﺗﺠﺮﺑﻲ ﻣﺴﺎﻓﺖ 1/5ﻣﺎﻳﻞ را ﺑﺎ ﺳﺮﻋﺖ ﺛﺎﺑﺖ
داﻧﺸﻜﺪه ﺗﺮﺑﻴﺖ ﺑﺪﻧﻲ و ﻋﻠﻮم ورزﺷﻲ ،داﻧﺸﮕﺎه ﻓﺮدوﺳﻲ ﻣﺸﻬﺪ ،ﻣﺸﻬﺪ ،اﻳﺮان.
)VO2max
(%70دوﻳﺪﻧﺪ و ﮔﺮوه ﻛﻨﺘﺮل ﻧﻴﺰ در اﻳﻦ ﻣﺪت ﺑﺪون ﺗﻤﺮﻳﻦ )ﺣﺎﺿﺮ در ﺷﺮاﻳﻂ ﺗﻤﺮﻳﻦ( ﺑﻮدﻧﺪ .ﻧﻤﻮﻧﻪﻫﺎي
ﺧﻮﻧﻲ ﻗﺒﻞ از ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ ﺑﻪﺻﻮرت ﻧﺎﺷﺘﺎ و ﺑﻼﻓﺎﺻﻠﻪ ﭘﺲ از ﺗﻤﺮﻳﻦ ،ﺑﻪﻣﻴﺰان 10mlاز ورﻳﺪ ﺑﺎزوﻳﻲ ﺟﻤﻊآوري ﺷﺪ .ﭘﺲ از ﺟﺪاﺳﺎزي ﻟﻨﻔﻮﺳﻴﺖﻫﺎ ﺑﻪروش ﺳﺎﻧﺘﺮﻳﻔﻴﻮژ ،ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در ﻟﻨﻔﻮﺳﻴﺖﻫﺎي آزﻣﻮدﻧﻲﻫﺎ ﺑﺎ اﺳﺘﻔﺎده از روش
Semi-quantitative-RT-PCR
اﻧﺠﺎم ﺷﺪ .ﻳﺎﻓﺘﻪﻫﺎ :اﻳﻦ ﭘﮋوﻫﺶ ﻧﺸﺎن داد ﻛﻪ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﻣﻮﺟﺐ
اﻓﺰاﻳﺶ اﻧﺪك ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖﻫﺎي آزﻣﻮدﻧﻲﻫﺎي ﮔﺮوه ﺗﺠﺮﺑﻲ ﻣﻲﺷﻮد ﻛﻪ اﻳﻦ اﻓﺰاﻳﺶ ﻧﺴﺒﺖ ﺑﻪ ﮔﺮوه ﻛﻨﺘﺮل ،ﺗﻐﻴﻴﺮات ﻣﻌﻨﻲداري را ﻧﺸﺎن ﻧﻤﻲدﻫﺪ .ﻧﺘﻴﺠﻪﮔﻴﺮي :ﻧﺘﺎﻳﺞ اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻣﺸﺨﺺ ﻣﻲﻛﻨﺪ ﻛﻪ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي اﻓﺰاﻳﺶ ﻣﻌﻨﻲداري در ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ اﻳﺠﺎد ﻧﻤﻲﻛﻨﺪ .ﻣﻤﻜﻦ اﺳﺖ ﺷﺪت ،ﻧﻮع و ﻣﺪت ﭘﺮوﺗﻜﻞ *
ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﻣﺸﻬﺪ ،ﻣﻴﺪان آزادي ،داﻧﺸﮕﺎه
ﻓﺮدوﺳﻲ ﻣﺸﻬﺪ ،داﻧﺸﻜﺪه ﺗﺮﺑﻴﺖ ﺑﺪﻧﻲ و ﻋﻠﻮم ورزﺷﻲ، ﮔﺮوه ﻓﻴﺰﻳﻮﻟﻮژي ورزﺷﻲ .ﻛﺪ ﭘﺴﺘﻲ9177948979 :
ﺗﻤﺮﻳﻨﻲ ﺑﻪﻛﺎر رﻓﺘﻪ در اﻳﻦ ﺗﺤﻘﻴﻖ ،ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ را ﺗﺤﺖ ﺗﺄﺛﻴﺮ ﻗﺮار ﻧﺪاده ﻛﻪ اﻳﻦ ﻧﺘﻴﺠﻪ ،ﻫﻢراﺳﺘﺎ ﺑﺎ ﻧﺘﺎﻳﺞ ﺳﺎﻳﺮ ﻣﻄﺎﻟﻌﺎت اﻧﺠﺎم ﺷﺪه در زﻣﻴﻨﻪ ﺗﻐﻴﻴﺮات ﭘﻼﺳﻤﺎﻳﻲ اﺑﺴﺘﺎﺗﻴﻦ ﻣﻲﺑﺎﺷﺪ.
ﺗﻠﻔﻦ0511-8829580 : E-mail: rashidlamir@ferdowsi.um.ac.ir
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :اﺑﺴﺘﺎﺗﻴﻦ ،ﺑﻴﺎن ژن ،ﻟﻨﻔﻮﺳﻴﺖ ،ﺗﻤﺮﻳﻦ ﻫﻮازي.
ﻏﺬا را ﻛﺎﻫﺶ ﻣﻲدﻫﺪ ،از ﺗﺨﻠﻴﻪ ﻣﻌﺪه و ﻓﻌﺎﻟﻴﺖ اﻧﻘﺒﺎﺿﻲ ژژﻧﻮم
ﻣﻘﺪﻣﻪ
ﺟﻠﻮﮔﻴﺮي ﻣﻲﻧﻤﺎﻳﺪ و در ﻛﺎﻫﺶ وزن ﺑﺪن ﻣﻮﺛﺮ ﻣﻲﺑﺎﺷﺪ .ﻧﺸﺎن داده
ﮔﺮﻟﻴﻦ ) ،(Ghrelinﻳﻚ ﭘﭙﺘﻴﺪ 28اﺳﻴﺪ آﻣﻴﻨﻪاي اﺳﺖ ﻛﻪ از ﻣﺨﺎط 2و1
و ﺑﻪﻋﻨﻮان ﻳﻚ ﻋﺎﻣﻞ
ﻣﻮﺛﺮ در ﺗﻨﻈﻴﻢ ﻣﻐﺰي -رودهاي ﻫﻮرﻣﻮن رﺷﺪ
Growth Hormone
ﻣﻌﺪه و روده اﻧﺴﺎن و ﻣﻮش ﺗﺮﺷﺢ ﻣﻲﮔﺮدد )(GH
و ﺗﻌﺎدل اﻧﺮژي ﺷﻨﺎﺧﺘﻪ ﺷﺪه اﺳﺖ4.و 3ﻋﻼوه ﺑﺮ ﮔﺮﻟﻴﻦ ،اﺑﺴﺘﺎﺗﻴﻦ
) (Obestatinﻳﻚ ﭘﭙﺘﻴﺪ 23اﺳﻴﺪ آﻣﻴﻨﻪاي اﺳﺖ ﻛﻪ از ﻓﻮﻧﺪوس ﻣﻌﺪه و ﻣﺨﺎط روده ﺗﺮﺷﺢ و ﺗﻮﺳﻂ ژن ﮔﺮﻟﻴﻦ ،ﻛﺪﮔﺬاري ﻣﻲﺷﻮد.
5-7
اﻛﺜﺮ
ﺷﺪه ﻛﻪ اﺑﺴﺘﺎﺗﻴﻦ ﺗﺮﺷﺢ ﻫﻮرﻣﻮن رﺷﺪ ﺗﻮﺳﻂ ﺳﻠﻮلﻫﺎي ﻫﻴﭙﻮﻓﻴﺰي را 8و7
ﻓﻌﺎﻟﻴﺖ ﺑﻴﻮﻟﻮژﻳﻜﻲ و ﺗﻮزﻳﻊ اﺑﺴﺘﺎﺗﻴﻦ و
در ﻣﻮشﻫﺎ ،ﺗﻐﻴﻴﺮ ﻧﺪاد.
ﻫﻢﭼﻨﻴﻦ ﻧﻘﺶ آن در ﺗﻌﺎدل اﻧﺮژي ،ﺗﺮﺷﺢ 10و9
ﺟﻮﻧﺪﮔﺎن ﻣﻄﺎﻟﻌﻪ ﺷﺪه اﺳﺖ.
GH
و وزن ﺑﺪن ،در
در اﻳﻦ ﺑﺎره ،اﻃﻼﻋﺎت ﻣﺘﻨﺎﻗﻀﻲ وﺟﻮد
دارد ،ﺑﺮﺧﻲ از ﻣﻄﺎﻟﻌﺎت ﮔﺰارش ﻛﺮدهاﻧﺪ ﻛﻪ اﺑﺴﺘﺎﺗﻴﻦ ﺟﺬب ﻏﺬا را ﻛﺎﻫﺶ ﻣﻲدﻫﺪ
4-7
و ﺳﺎﻳﺮ ﻣﻄﺎﻟﻌﺎت ،اﻋﻼم ﻛﺮدهاﻧﺪ ﻛﻪ اﺑﺴﺘﺎﺗﻴﻦ ﻫﻴﭻ 8-11
ﺗﺤﻘﻴﻘﺎت ﭘﻴﺸﻨﻬﺎد ﻣﻲﻛﻨﻨﺪ ﻛﻪ اﮔﺮ ﭼﻪ ﮔﺮﻟﻴﻦ و اﺑﺴﺘﺎﺗﻴﻦ از ﭘﻴﺶ
اﺛﺮي ﺑﺮ ﺟﺬب ﻏﺬا ﻧﺪارد.
ﺳﺎﺧﺖ ﭘﺮوﭘﭙﺘﻴﺪي ﻳﻜﺴﺎﻧﻲ ﻣﻨﺸﺎ ﻣﻲﮔﻴﺮﻧﺪ ،اﻳﻦ دو ﻫﻮرﻣﻮن ﻧﻘﺶﻫﺎي
ﻣﻴﺰان ﺣﺮﻛﺎت ﻣﻌﺪي -رودهاي ،ﻫﻤﻮﺳﺘﺎز ﮔﻠﻮﻛﺰ ،ﺗﻜﺜﻴﺮ ﺳﻠﻮﻟﻲ ،ﺗﺮﺷﺢ
ﻓﻴﺰﻳـﻮﻟﻮژﻳﻜﻲ ﻣﺘﻀﺎدي دارﻧﺪ8.و 7در ﻣﻘﺎﻳـﺴﻪ ﺑﺎ ﮔﺮﻟﻴﻦ ،اﺑﺴﺘﺎﺗﻴﻦ ﺟﺬب
ﻫﻮرﻣﻮن ،ﺗﺸﻨﮕﻲ ،ﺧﻮاب ،ﺣﺎﻓﻈﻪ ،اﺿﻄﺮاب ،ﺟﺬب آب ،وزن ﺑﺪن و
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻣﻄﺎﻟﻌﺎت ﻧﺸﺎن ﻣﻲدﻫﺪ ﻛﻪ اﺑﺴﺘﺎﺗﻴﻦ ﺑﺮ
اﻣﻴﺮ رﺷﻴﺪﻟﻤﻴﺮ و ﻫﻤﻜﺎران
8-12
ﻫﺰﻳﻨﻪ اﻧﺮژي ﺗﺄﺛﻴﺮ دارد.
ﺑﺮ ﻃﺒﻖ ﺷﻮاﻫﺪ ،اﺑﺴﺘﺎﺗﻴﻦ در وﺿﻌﻴﺖ 13
ﻣﻘﺎوﻣﺖ ﺑﻪ اﻧﺴﻮﻟﻴﻦ ،ﻛﺎﻫﺶ ﻣﻲﻳﺎﺑﺪ و ﻋﻤﻠﻜﺮد ﮔﺮﻟﻴﻦ را در ﺑﺪن 10
ﺗﻌﺪﻳﻞ ﻣﻲﻧﻤﺎﻳﺪ.
ﻏﻠﻈﺖ اﺑﺴﺘﺎﺗﻴﻦ ﭘﻼﺳﻤﺎ ﺑﻪوﺳﻴﻠﻪ ﮔﺮﺳﻨﮕﻲ و
ﺳﻴﺮي 14،وﻋﺪه ﻏﺬاﻳﻲ ﭘﺮ ﻛﺮﺑﻮﻫﻴﺪرات 15،ﻛﺎﻫﺶ وزن 16و ﭼﺎﻗﻲ
427
وزن آزﻣﻮدﻧﻲﻫﺎ از ﺗﺮازوي دﻳﺠﻴﺘﺎﻟﻲ ﺑﺎ ﺣﺴﺎﺳﻴﺖ 0/1ﻛﻴﻠﻮﮔﺮم اﺳﺘﻔﺎده ﺷﺪ و آزﻣﻮدﻧﻲﻫﺎ ﻗﺒﻞ از ﻧﻤﻮﻧﻪﮔﻴﺮي اوﻟﻴﻪ وزنﻛﺸﻲ ﺷﺪﻧﺪ .ﺿﺮﺑﺎن ﻗﻠﺐ آزﻣﻮدﻧﻲﻫﺎ ﺗﻮﺳﻂ دﺳﺘﮕﺎه ﺿﺮﺑﺎن ﺳﻨﺞ ﭘﻮﻻر ﻣﺪل
F1tm
ﺳﺎﺧﺖ
18و17
ﻛﺸﻮر ﻓﻨﻼﻧﺪ اﻧﺪازهﮔﻴﺮي ﺷﺪ .ﻫﻢﭼﻨﻴﻦ زﻣﺎن ﺗﻤﺮﻳﻦ ﺗﻮﺳﻂ ﻛﺮﻧﻮﻣﺘﺮ
ﺗﻨﻈﻴﻢ ﻣﻲﮔﺮدد .از آﻧﺠﺎﻳﻲﻛﻪ ﮔﺮﻟﻴﻦ و اﺑﺴﺘﺎﺗﻴﻦ ﺑﺮ ﺗﻌﺎدل اﻧﺮژي ﻣﺆﺛﺮ
دﻳﺠﻴﺘﺎل ﺑﺎ دﻗﺖ 0/01ﺛﺎﻧﻴﻪ اﻧﺪازهﮔﻴﺮي ﺷﺪ .درﺻﺪ ﭼﺮﺑﻲ آزﻣﻮدﻧﻲﻫﺎ
ﻫﺴﺘﻨﺪ ،ﻣﺸﺨﺺ ﻧﻤﻮدن اﺛﺮات ﺗﻤﺮﻳﻦ ﺑﺪﻧﻲ ﺑﺮ اﻳﻦ ﻫﻮرﻣﻮنﻫﺎ ﺿﺮوري
ﺑﺎ اﺳﺘﻔﺎده از ﻛﺎﻟﻴﭙﺮ و ﺑﺎ اﺳﺘﻔﺎده از ﻓﺮﻣﻮل ﺳﻪ ﻧﻘﻄﻪاي
Dale Wagner
ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ .ﻣﻄﺎﻟﻌﺎت درﺑﺎره اﺛﺮ ﺑﺮﻧﺎﻣﻪ ﺗﻤﺮﻳﻨﻲ ﺑﺮ اﺑﺴﺘﺎﺗﻴﻦ ،ﺑﻪوﻳﮋه
اﻧﺪازهﮔﻴﺮي ﺷﺪ .وﻳﮋﮔﻲﻫﺎي آزﻣﻮدﻧﻲﻫﺎي ﺗﺤﻘﻴﻖ در ﺟﺪول 1آورده
در اﻧﺴﺎنﻫﺎ ،ﺑﺴﻴﺎر اﻧﺪك و ﻣﺤﺪود اﺳﺖ .در ﻳﻚ ﻣﻄﺎﻟﻌﻪ اﺛﺮ ﻳﻚ ﺟﻠﺴﻪ
ﺷﺪه اﺳﺖ .از ﺗﻤﺎﻣﻲ آزﻣﻮدﻧﻲﻫﺎ ﻗﺒﻞ از اﻧﺠﺎم ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ و ﭘﺲ
ﺗﻤﺮﻳﻦ ﻣﻘﺎوﻣﺘﻲ داﻳﺮهاي ﺑﺎ ﺷﺪتﻫﺎي ﻣﺨﺘﻠﻒ ﺑﺮ ﺳﻄﻮح ﭘﻼﺳﻤﺎﻳﻲ
از ﻧﺎﺷﺘﺎﻳﻲ 12ﺳﺎﻋﺘﻪ در ﺳﺎﻋﺖ ﻫﺸﺖ ﺻﺒﺢ و ﻫﻢﭼﻨﻴﻦ ﺑﻼﻓﺎﺻﻠﻪ ﺑﻌﺪ
ﮔﺰارش ﺷﺪه اﺳﺖ 19.در ﻣﻄﺎﻟﻌﻪاي دﻳﮕﺮ اﺛﺮ ﺷﺶ ﻫﻔﺘﻪ ﺗﻤﺮﻳﻦ ﺗﺮدﻣﻴﻞ
از اﺗﻤﺎم ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ ،ﻫﺮ ﺑﺎر ﺑﻪﻣﻴﺰان 10mlاز ورﻳﺪ ﺑﺎزوﻳﻲ ﺧﻮن-
ﺑﺮ ﻏﻠﻈﺖ ﻛﻞ اﺑﺴﺘﺎﺗﻴﻦ ﻓﻮﻧﺪوس و روده ﻛﻮﭼﻚ در ﻣﻮشﻫﺎ ﺑﺮرﺳﻲ
ﮔﻴﺮي ﺑﻪﻋﻤﻞ آﻣﺪ .ﻧﻤﻮﻧﻪﻫﺎي ﺧﻮﻧﻲ در ﻟﻮﻟﻪﻫﺎي آزﻣﺎﻳﺸﻲ ﺑﺎ ﻣﺎده ﺿﺪ
ﺷﺪه اﺳﺖ 20.اﻣﺎ ﺑﺎ ﺑﺮرﺳﻲﻫﺎي ﺑﻪﻋﻤﻞ آﻣﺪه ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ ﺗﺎ اﻳﻦ زﻣﺎن
اﻧﻌﻘﺎد
ﺗﺤﻘﻴﻘﻲ ﻣﺒﻨﻲ ﺑﺮ ﺗﺄﺛﻴﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در
ﻟﻨﻔﻮﺳﻴﺖﻫﺎ ﺑﻪروش ﺳﺎﻧﺘﺮﻳﻔﻴﻮژ در اﻳﻦ ﻣﺮﺣﻠﻪ اﻧﺠﺎم ﺷﺪ .ﺑﺮاي
ﻟﻨﻔﻮﺳﻴﺖ آزﻣﻮدﻧﻲﻫﺎي اﻧﺴﺎﻧﻲ ،ﻣﻨﺘﺸﺮ ﻧﺸﺪه اﺳﺖ .ﺑﻨﺎﺑﺮاﻳﻦ ،در اﻳﻦ
اﻧﺪازهﮔﻴﺮي ﻣﻴﺰان ﺑﻴﺎن mRNAاز روش
Semi quantitative RT-PCR
ﺗﺤﻘﻴﻖ ﺑﺮرﺳﻲ ﻛﺮدهاﻳﻢ ﻛﻪ آﻳﺎ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺳﺒﺐ اﻓﺰاﻳﺶ
اﺳﺘﻔﺎده ﺷﺪ .ﺑﺪﻳﻦﺻﻮرت ﻛﻪ ﻟﻨﻔﻮﺳﻴﺖﻫﺎ را در ﻧﻴﺘﺮوژن ﻣﺎﻳﻊ ﻗﺮار داده
ﻣﻌﻨﻲداري در ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ اﻧﺴﺎﻧﻲ ﻣﻲﮔﺮدد.
و ﺑﻪﺻﻮرت ﻛﺎﻣﻞ ﺗﻮﺳﻂ Mortal & Pestleﺧﺮد ﻛﺮدﻳﻢ .ﺑﺎﻓﺖ ﺗﺨﺮﻳﺐ
EDTA
ﺟﻤﻊآوري و ﺑﻪ آزﻣﺎﻳﺸﮕﺎه اﻧﺘﻘﺎل داده ﺷﺪ ،ﺟﺪاﺳﺎزي
ﺷﺪه در ﺑﺎﻓﺮ RLTﻫﻤﻮژﻧﻴﺰه ﺷﺪ ،اﺳﺘﻔﺎده از ﻫﻤﻮژنﻛﻨﻨﺪه
Rotor-stator
روش ﺑﺮرﺳﻲ
ﻣﻮﺟﺐ ﻓﺮاﻫﻢ ﺷﺪن ﻣﻘﺎدﻳﺮ ﺑﻴﺸﺘﺮي از
ﻃﺮح ﺗﺤﻘﻴﻖ ﺣﺎﺿﺮ دو ﮔﺮوﻫﻲ ﺑﺎ ﭘﻴﺶآزﻣﻮن و ﭘﺲآزﻣﻮن ﺑﻮده و از
ﻧﻴﺘﺮوژن ﻣﺎﻳﻊ ،در ﺗﻴﻮب ﻣﻴﻜﺮوﺳﺎﻧﺘﺮﻳﻔﻴﻮژ 2ml ،RNase freeرﻳﺨﺘﻪ ﺷﺪ
ﻧﻮع ﺗﺤﻘﻴﻘﺎت ﻧﻴﻤﻪﺗﺠﺮﺑﻲ ﻣﻲﺑﺎﺷﺪ .آزﻣﻮدﻧﻲﻫﺎي اﻳﻦ ﺗﺤﻘﻴﻖ ﺷﺎﻣﻞ 16
و اﺟﺎزه داده ﺷﺪ ﺗﺎ ﻧﻴﺘﺮوژن ﻣﺎﻳﻊ ﺗﺒﺨﻴﺮ ﺷﻮد وﻟﻲ ﻟﻨﻔﻮﺳﻴﺖﻫﺎ از ﺣﺎﻟﺖ
زن ﺳﺎﻟﻢ ﺑﻮدﻧﺪ ﻛﻪ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻓﺮاﺧﻮان ﻣﺤﻘﻘﻴﻦ از ﺟﺎﻣﻌﻪ ورزشﻛﺎران
ﻳﺦزدﮔﻲ ﺧﺎرج ﻧﺸﻮد .ﺑﻪﻣﻴﺰان ﻛﺎﻓﻲ ﺑﺎﻓﺮ
اﺿﺎﻓﻪ ﺷﺪ Lysate .را
اﺳﺘﺎن ﺧﺮاﺳﺎن رﺿﻮي )ﺗﺎﺑﺴﺘﺎن ﺳﺎل (1389اﻧﺘﺨﺎب و ﭘﺲ از اﻧﺠﺎم
ﻣﺴﺘﻘﻴﻢ ﺑﻪﺳﺘﻮن QIAshredderﻛﻪ در ﺗﻴﻮب ﻗﺮار داﺷﺖ ،ﻣﻨﺘﻘﻞ ﻛﺮده و
ﻣﻌﺎﻳﻨﺎت ﭘﺰﺷﻜﻲ و ﺗﻌﻴﻴﻦ ﺳﻼﻣﺖ ﻛﺎﻣﻞ ﺟﺴﻤﺎﻧﻲ ﺗﻮﺳﻂ ﭘﺰﺷﻚ و
ﺑﻪﻣﺪت دو دﻗﻴﻘﻪ و ﺑﺎ ﺳﺮﻋﺖ ﺑﺎﻻ ﺳﺎﻧﺘﺮﻳﻔﻴﻮژ ﻛﺮدﻳﻢ ،ﺳﭙﺲ ﻣﻮاد وارد
ﻛﺴﺐ رﺿﺎﻳﺖﻧﺎﻣﻪ ﺟﻬﺖ ﺷﺮﻛﺖ در ﭘﮋوﻫﺶ و ﻧﻤﻮﻧﻪﮔﻴﺮي ﺧﻮﻧﻲ ،ﺑﻪ
دﺳﺘﮕﺎه PCRﺷﺪه و در اﻧﺘﻬﺎ روي ژل آﮔﺎرز ﻗﺮار ﮔﺮﻓﺘﻨﺪ ﺗﺎ ﻋﻜﺲﻫﺎي
ﻃﻮر ﺗﺼﺎدﻓﻲ ﺑﻪ دو ﮔﺮوه ﻛﻨﺘﺮل و ﺗﺠﺮﺑﻲ )ﻫﺮ ﮔﺮوه ﻫﺸﺖ ﻧﻔﺮ( ﺗﻘﺴﻴﻢ
ﻻزم از آنﻫﺎ ﺗﻬﻴﻪ ﺷﻮد .در اﻧﺘﻬﺎ ﭘﺲ از ﺑﻪدﺳﺖ آﻣﺪن ﻧﺘﺎﻳﺞ ﺑﺎ اﺳﺘﻔﺎده
ﺷﺪﻧﺪ .ﺗﻤﺎﻣﻲ آزﻣﻮدﻧﻲﻫﺎ ﺑﻪﻃﻮر ﻛﺎﻣﻞ ﺑﺎ ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ آﺷﻨﺎ ﺷﺪﻧﺪ.
از دﺳﺘﮕﺎه
ﻣﺪل Gel Doc-It Ts310ﺳﺎﺧﺖ ﻛﺸﻮر آﻣﺮﻳﻜﺎ و
ﺗﻤﺎﻣﻲ آزﻣﻮدﻧﻲﻫﺎ در زﻣﺎن اﻧﺠﺎم ﭘﺮوﺗﻜﻞ در دوره ﻟﻮﺗﺌﺎل ﻗﺮار داﺷﺘﻨﺪ.
ﺑﻪدﺳﺖ آوردن ﻣﻘﺎدﻳﺮ ﺑﺘﺎ اﻛﺘﻴﻦ ﺑﺮاي ﻫﺮ ﻧﻤﻮﻧﻪ ،ﻋﺪدﻫﺎي ﺑﻪدﺳﺖ آﻣﺪه
ﻣﻴﺎﻧﮕﻴﻦ ﻛﺎﻟﺮي ﻣﺼﺮﻓﻲ آزﻣﻮدﻧﻲﻫﺎ از ﻃﺮﻳﻖ ﭘﺮﺳﺶﻧﺎﻣﻪ ﺳﻪ روزه رژﻳﻢ
را ﺑﺮ ﻣﻘﺎدﻳﺮ ﺑﺘﺎاﻛﺘﻴﻦ ﺑﺮاي ﻫﺮ ﻳﻚ ،ﺗﻘﺴﻴﻢ ﻧﻤﻮدﻳﻢ و ﺣﺎﺻﻞ را در 100
UVP
RNA
RLT
ﻣﻲﺷﻮد .ﭘﻮدر ﺑﺎﻓﺖ و
ﻏﺬاﻳﻲ و ﺑﺎ اﺳﺘﻔﺎده از ﺟﺪولﻫﺎي ﻣﺮﺑﻮﻃﻪ ﻣﺤﺎﺳﺒﻪ ﮔﺮدﻳﺪ و ﺑﺮ ﻃﺒﻖ آن وﻋﺪه ﻏﺬاﻳﻲ ﺷﺐ ﭘﻴﺶ از ﺧﻮنﮔﻴﺮي ﺗﻬﻴﻪ و ﺑﻪ ﺗﻤﺎم آزﻣﻮدﻧﻲﻫﺎ ﺗﺤﻮﻳﻞ داده ﺷﺪ .ﺑﺮاي ﻛﻨﺘﺮل رژﻳﻢ ﻏﺬاﻳﻲ آزﻣﻮدﻧﻲﻫﺎ و ﺟﻠﻮﮔﻴﺮي از ﺗﺪاﺧﻞ رژﻳﻢ ﻏﺬاﻳﻲ ﺑﺮ ﻣﻘﺎدﻳﺮ ﻣﻮرد اﻧﺪازهﮔﻴﺮي ﻗﺒﻞ از ﺧﻮنﮔﻴﺮي ﺑﻪ آزﻣﻮدﻧﻲﻫﺎ ﺗﻮﺻﻴﻪ ﺷﺪه ﺑﻮد ﺗﺎ ﺑﻪﻣﺪت 12ﺳﺎﻋﺖ از ﺧﻮردن ﭘﺮﻫﻴﺰ ﻛﻨﻨﺪ ،اﻟﺒﺘﻪ آزﻣﻮدﻧﻲﻫﺎ ﻣﺠﺎز ﺑﻪ ﻧﻮﺷﻴﺪن آب ﺑﻮدﻧﺪ .ﺑﺮاي اﻧﺪازهﮔﻴﺮي
ﺟﺪول :1-وﻳﮋﮔﻲﻫﺎي آﻧﺘﺮوﭘﻮﻣﺘﺮﻳﻚ آزﻣﻮدﻧﻲﻫﺎ ﮔﺮوه
ﻣﻴﺎﻧﮕﻴﻦ ﻗﺪ
ﻣﻴﺎﻧﮕﻴﻦ وزن
BMI
FB%
ﻛﻨﺘﺮل
161±2/29
61/65±10/05
23/88±4/66
22/156
ﻫﻮازي
158±3/6
49/88±4/7
19/98±1/955
22/750
) FB%: Body Fat percentدرﺻﺪ ﭼﺮﺑﻲ ﺑﺪن() BMI: Body Mass Index ،ﺷﺎﺧﺺ ﺗﻮده ﺑﺪن(
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
428
ﺗﺄﺛﻴﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ در زﻧﺎن ﺗﻤﺮﻳﻦ ﻛﺮده
ﺿﺮب ﻧﻤﻮدﻳﻢ ﺗﺎ ﻣﻘﺎدﻳﺮ mRNAي اﺑﺴﺘﺎﺗﻴﻦ ﺑﺮاي ﻫﺮ ﻧﻤﻮﻧﻪ ﺑﺮاﺳﺎس درﺻﺪ ﺑﻪدﺳﺖ آﻳﺪ .ﺗﻐﻴﻴﺮات ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﺑﻪروش
RT-PCR
ﻧﻴﻤﻪ ﻛﻤﻲ اﻧﺪازهﮔﻴﺮي ﺷﺪ .اﻳﻦ روش ﺑﻪﻛﻤﻚ ﭘﺮاﻳﻤﺮﻫﺎي وﻳﮋه اﺑﺴﺘﺎﺗﻴﻦ ﺷﺎﻣﻞ
AGCCCTGAACACCAGAGAGTC
،OBESTATIN-f
OBESTATIN-r CCAGAGGATGTCCTGAAGAAAC
ﺟﺪول :2-ﺗﻐﻴﻴﺮات ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در ﮔﺮوهﻫﺎ ﮔﺮوه
ﭘﻴﺶآزﻣﻮن
ﭘﺲآزﻣﻮن
*P
ﻫﻮازي
35/57±22/56
46/72±17/31
0/473
ﻛﻨﺘﺮل
59/85±16/50
66/18±14/62
0/860
* Paired sample t-test
**P
0/792
** Independent sample t-test
ﻛﻪ ﻳﻚ ﻗﻄﻌﻪ
237ﺑﺎزي را در اﻳﻦ ژن ﺗﻜﺜﻴﺮ ﻣﻲﻛﻨﻨﺪ ،اﻧﺠﺎم ﺷﺪ. از آزﻣﻮدﻧﻲﻫﺎي ﮔﺮوه ﺗﺠﺮﺑﻲ ﺧﻮاﺳﺘﻪ ﺷﺪ ﺗﺎ ﻣﺴﺎﻓﺖ 1/5ﻣﺎﻳﻞ را ﺑﺎ ﺳﺮﻋﺖ ﺛﺎﺑﺖ
)VO2max
21-23
(%70ﺑﺪوﻧﺪ.
ﭘﻴﺶ از ﭘﺮوﺗﻜﻞ 5-10
دﻗﻴﻘﻪ زﻣﺎن ﺑﻪ ﮔﺮم ﻛﺮدن و ﺣﺪود 10دﻗﻴﻘﻪ ﺑﻪ ﺳﺮد ﻛﺮدن ﭘﺲ از ﭘﺮوﺗﻜﻞ اﺧﺘﺼﺎص ﻳﺎﻓﺖ .ﻛﻞ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ و ﻧﻤﻮﻧﻪﮔﻴﺮي از ﺳﺎﻋﺖ 9 ﺗﺎ 11/5ﻇﻬﺮ ﺑﻪﻃﻮل اﻧﺠﺎﻣﻴﺪ .ﺗﻤﺎم ﺷﺮﻛﺖﻛﻨﻨﺪﮔﺎن ﭘﺲ از ﻧﺎﺷﺘﺎﻳﻲ ﺷﺐ ﻗﺒﻞ )ﺣﺪاﻗﻞ 12ﺳﺎﻋﺖ ،ﻓﻘﻂ اﺟﺎزه ﻧﻮﺷﻴﺪن آب داﺷﺘﻨﺪ( ﺑﻪ
ﺷﻜﻞ :1-اﻟﻜﺘﺮوﻓﻮرز از ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در ﮔﺮوه ﻛﻨﺘﺮل
آزﻣﺎﻳﺸﮕﺎه ﻣﻨﺘﻘﻞ ﺷﺪﻧﺪ .از آزﻣﻮدﻧﻲﻫﺎ ﺧﻮاﺳﺘﻪ ﺷﺪ ﺿﻤﻦ رﻋﺎﻳﺖ رژﻳﻢ ﻏﺬاﻳﻲ ،از ﺗﻤﺮﻳﻦ ﻛﺮدن در ﺑﺎزه زﻣﺎﻧﻲ ﺳﻪ روز ﭘﻴﺶ از ﺗﻤﺮﻳﻦ ﭘﺮﻫﻴﺰ ﻛﻨﻨﺪ ،ﻫﻢﭼﻨﻴﻦ در اﻳﻦ ﻣﺪت ﻫﻴﭻ داروﻳﻲ ﻣﺼﺮف ﻧﻜﻨﻨﺪ .ﻣﺤﺎﺳﺒﻪﻫﺎي آﻣﺎري ﺑﺎ ﻧﺮماﻓﺰار SPSSوﻳﺮاﺳﺖ 16اﻧﺠﺎم ﺷﺪ .از آﻣﺎر ﺗﻮﺻﻴﻔﻲ ﺑﺮاي دﺳﺘﻪﺑﻨﺪي دادهﻫﺎ و ﺑﺮاي ﺗﺠﺰﻳﻪ و ﺗﺤﻠﻴﻞ دادهﻫﺎ از آزﻣﻮن Independent sample t-testاﺳﺘﻔﺎده ﺷﺪ .ﺳﻄﺢ ﻣﻌﻨﻲداري آﻣﺎري P<0/01در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﺷﺪ.
ﺷﻜﻞ :2-اﻟﻜﺘﺮوﻓﻮرز از ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در ﮔﺮوه ﺗﺠﺮﺑﻲ
ﻳﺎﻓﺘﻪﻫﺎ ﻧﺘﺎﻳﺞ ﺗﺤﻘﻴﻖ ﺣﺎﺿﺮ ﻧﺸﺎن داد ﻛﻪ ﺑﻼﻓﺎﺻﻠﻪ ﭘﺲ از ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ، ﻋﻠﻲرﻏﻢ اﻓﺰاﻳﺶ اﻧﺪك اﺑﺴﺘﺎﺗﻴﻦ در ﮔﺮوه ﻫﻮازي )ﻧﻤﻮدار 1و ﺟﺪول
ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در ﻟﻨﻔﻮﺳﻴﺖﻫﺎ ﻣﺸﺎﻫﺪه ﻧﮕﺮدﻳﺪ )ﺑﻪﺗﺮﺗﻴﺐ
P<0/473
و .(P<0/860
،(2در ﻫﻴﭻﻳـﻚ از ﮔـﺮوهﻫﺎي ﻫـﻮازي و ﻛﻨﺘﺮل اﻓﺰاﻳﺶ ﻣﻌﻨﻲداري در
ﺑﺤﺚ ﻫﺪف از ﭘﮋوﻫﺶ ﺣﺎﺿﺮ ﺑﺮرﺳﻲ اﺛﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ زﻧﺎن ﺗﻤﺮﻳﻦ ﻛﺮده ﺑﻮد .ﻧﺘﺎﻳﺞ ﺗﺤﻘﻴﻖ ﺣﺎﺿﺮ ﻧﺸﺎن داد ﻛﻪ ﻳﻚ وﻫﻠﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺳﺒﺐ اﻓﺰاﻳﺶ ﻣﻌﻨﻲداري در ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖﻫﺎ ﻧﻤﻲﮔﺮدد .در اﻳﻦ زﻣﻴﻨﻪ Ghanbari-Niaki ،ﺑﻪ ﺑﺮرﺳﻲ اﺛﺮ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﺑﺎ ﺷﺪتﻫﺎي ﻣﺨﺘﻠﻒ ﺑﺮ ﺳﻄﻮح ﭘﻼﺳﻤﺎﻳﻲ اﺑﺴﺘﺎﺗﻴﻦ ﭘﺮداﺧﺖ ،ﻧﺘﺎﻳﺞ اﻳﻦ ﭘﮋوﻫﺶ ﺣﺎﻛﻲ از آن ﺑﻮد ﻛﻪ ﺳﻄﻮح اﺑﺴﺘﺎﺗﻴﻦ ﭘﻼﺳﻤﺎ در ﭘﺎﺳﺦ ﺑﻪ ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻣﻘﺎوﻣﺘﻲ در ﻫﻴﭻﻳﻚ از ﺷﺪتﻫﺎي ﻣﺨﺘﻠﻒ ﺗﻤﺮﻳﻦ ،ﺗﻐﻴﻴﺮ ﻣﻌﻨﻲداري ﻧﻴﺎﻓﺖ. ﻧﻤﻮدار :1-ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ در دو ﮔﺮوه ﻗﺒﻞ و ﺑﻌﺪ اﺟﺮاي ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
19
Manshouriﺑﻪ ﺑﺮرﺳﻲ اﺛﺮ ﻳﻚ ﺑﺮﻧﺎﻣﻪ ﺗﻤﺮﻳﻦ ﺑﻲﻫﻮازي ﻛﻮﺗﺎهﻣﺪت ﺑﺮ
ﻫﻤﻜﺎران رﺷﻴﺪﻟﻤﻴﺮ و Rashidlamir A. etاﻣﻴﺮ al.
429
ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ.ﻟﻨﻔﻮﺳﻴﺖ در ﻫﻴﭻﻳﻚ از دو ﮔﺮوه ﻣﻌﻨﻲدار ﻧﺒﻮد
ﻧﺘﺎﻳﺞ اﻳﻦ ﭘﮋوﻫﺶ ﻧﺸﺎن داد،ﺳﻄﻮح ﭘﻼﺳﻤﺎﻳﻲ اﺑﺴﺘﺎﺗﻴﻦ ﭘﺮداﺧﺘﻪ اﺳﺖ
ﻳﻚ ﺗﻜﺮار ﺑﻴﺸﻴﻨﻪ ﺑﻪﻃﻮر%80 ﻧﺴﺒﺖ ﺳﻄﺢ ﮔﺮﻟﻴﻦ ﺑﻪ اﺑﺴﺘﺎﺗﻴﻦ در ﮔﺮوه
ﻛﻪ ﺳﻄﻮح اﺑﺴﺘﺎﺗﻴﻦ ﭘﻼﺳﻤﺎ در آزﻣﻮدﻧﻲﻫﺎ ﺗﻐﻴﻴﺮ ﻧﻴﺎﻓﺖ و ﭘﮋوﻫﺶﮔﺮان
ﺑﻪﻧﻈﺮ ﭘﮋوﻫﺶﮔﺮان اﻳﻦ اﻓﺮاﻳﺶ ﺑﻪﻃﻮر،ﻣﻌﻨﻲداري اﻓﺰاﻳﺶ ﻳﺎﻓﺘﻪ ﺑﻮد
ﻧﺘﻴﺠﻪﮔﻴﺮي ﻛﺮدﻧﺪ ﻛﻪ ﺳﻄﺢ اﺑﺴﺘﺎﺗﻴﻦ ﺗﺤﺖ ﺗﺎﺛﻴﺮ ﻓﻌﺎﻟﻴﺖﻫﺎي ورزﺷﻲ
اﺣﺘﻤﺎﻟﻲ ﺑﺮاي ﺗﺤﺮﻳﻚ درﻳﺎﻓﺖ ﻏﺬا و ﺟﺒﺮان ﻣﻨﺎﺑﻊ از دﺳﺖ رﻓﺘﻪ اﻧﺮژي
ﻫﻢﭼﻨﻴﻦ ﻳﻚ ﺑﺮﻧﺎﻣﻪ ﺗﻤﺮﻳﻦ ﺗﺮدﻣﻴﻞ ﺑﻪﻣﺪت24.ﻛﻮﺗﺎهﻣﺪت ﻗﺮار ﻧﻤﻲﮔﻴﺮد
ﮔﺮ ﭼﻪ ﺗﺤﻘﻴﻘﺎت اﻧﺪﻛﻲ درﺑﺎره ﺗﺄﺛﻴﺮ ﺗﻤﺮﻳﻦ26.ﺻﻮرت ﮔﺮﻓﺘﻪ اﺳﺖ
در ﺳﻄﻮح اﺑﺴﺘﺎﺗﻴﻦ ﭘﻼﺳﻤﺎي ﻣﻮشﻫﺎ22m/min ﻫﺸﺖ ﻫﻔﺘﻪ ﺑﺎ ﺷﺪت
ﻫﻴﭻ ﭘﮋوﻫﺸﻲ در،ﺑﺪﻧﻲ ﺑﺮ ﺳﻄﻮح ﭘﻼﺳﻤﺎﻳﻲ اﺑﺴﺘﺎﺗﻴﻦ اﻧﺠﺎم ﺷﺪه اﺳﺖ
در ﻳﻚ ﺗﺤﻘﻴﻖ ﺑﺮاي ﻛﺎﻫﺶ وزن، از ﻃﺮﻓﻲ25.ﺗﻐﻴﻴﺮي اﻳﺠﺎد ﻧﻜﺮد
راﺑﻄﻪ ﺑﺎ ﺗﺄﺛﻴﺮ ﻓﻌﺎﻟﻴﺖ ﺑﺪﻧﻲ ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ اﻧﺠﺎم ﻧﺸﺪه
رژﻳﻢ ﻏﺬاﻳﻲ ﺑﻪ اﺿﺎﻓﻪ ﻓﻌﺎﻟﻴﺖ ﺑﺪﻧﻲ ﺑﻪﻛﺎر،ﻛﻮدﻛﺎن داراي اﺿﺎﻓﻪ وزن
ﭘﮋوﻫﺶ ﺣﺎﺿﺮ ﻧﻘﺶ ﺗﻤﺮﻳﻦ ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﺑﻪروش.اﺳﺖ
ﻧﺘﺎﻳﺞ اﻳﻦ ﭘﮋوﻫﺶ ﻧﺸﺎن داد ﻛﻪ ﺗﺮﻛﻴﺐ رژﻳﻢ ﻏﺬاﻳﻲ،رﻓﺖ
ﻧﻴﻤﻪﺗﺠﺮﺑﻲ و ﺑﺎ اﺟﺮاي ﭘﺮوﺗﻜﻞ ﺗﻤﺮﻳﻨﻲ ﺑﺮاي اوﻟﻴﻦﺑﺎر روي اﻧﺴﺎن
ﻛﻢﭼﺮﺑﻲ و ﻓﻌﺎﻟﻴﺖ ﺑﺪﻧﻲ ﻣﻨﺠﺮ ﺑﻪ ﻛﺎﻫﺶ وزن ﺷﺪ و،ﭘﺮﻛﺮﺑﻮﻫﻴﺪرات
ﺳﺎز و ﻛﺎرﻫﺎي ﺗﺄﺛﻴﺮ ورزش ﺑﺮ ﺑﻴﺎن ژن ﻟﻨﻔﻮﺳﻴﺖ.اﻧﺠﺎم ﺷﺪه اﺳﺖ
در ﺣﺎﻟﻲ ﻛﻪ ﺳﻄﺢ ﮔﺮﻟﻴﻦ ﺗﻐﻴﻴﺮ،در ﻧﺘﻴﺠﻪ ﺳﻄﺢ اﺑﺴﺘﺎﺗﻴﻦ اﻓﺰاﻳﺶ ﻳﺎﻓﺖ
ﻫﻢراﺳﺘﺎ ﺑﺎ ﺳﺎﻳﺮ، ﻧﺘﺎﻳﺞ ﻣﺸﺎﻫﺪه ﺷﺪه در اﻳﻦ ﻣﻄﺎﻟﻌﻪ.ﻧﺎﺷﻨﺎﺧﺘﻪ اﺳﺖ
ﻣﻌﻨﻲداري ﻧﺪاﺷﺖ و ﭘﮋوﻫﺶﮔﺮان ﭼﻨﻴﻦ ﭘﻴﺸﻨﻬﺎد ﻛﺮدﻧﺪ ﻛﻪ ﻣﻤﻜﻦ
.ﻣﻄﺎﻟﻌﺎت اﻧﺠﺎمﺷﺪه در زﻣﻴﻨﻪ ﺗﻐﻴﻴﺮات ﭘﻼﺳﻤﺎﻳﻲ اﺑﺴﺘﺎﺗﻴﻦ ﻣﻲﺑﺎﺷﺪ
ﺳﺎز و ﻛﺎري ﺿﺮوري،اﺳﺖ اﻓﺰاﻳﺶ اﺑﺴﺘﺎﺗﻴﻦ ﺑﻪدﻧﺒﺎل ﻛﺎﻫﺶ وزن
ﻧﻮع و ﻣﺪت ﭘﺮوﺗﻜﻞ،ﭘﻴﺸﻨﻬﺎد داده ﻣﻲﺷﻮد ﻛﻪ ﻣﻤﻜﻦ اﺳﺖ ﺷﺪت
اﺛﺮ ﭼﻬﺎرSaghebjoo در ﭘﮋوﻫﺶ16.ﺑﺮاي ﺣﻔﻆ ﻛﺎﻫﺶ وزن ﺑﺎﺷﺪ
ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ را ﺗﺤﺖ ﺗﺄﺛﻴﺮ،ﻣﻮرد اﺳﺘﻔﺎده در اﻳﻦ ﺗﺤﻘﻴﻖ
ﻳﻚ ﺗﻜﺮار ﺑﻴﺸﻴﻨﻪ%80 و40 ﻫﻔﺘﻪ ﺗﻤﺮﻳﻦ ﻣﻘﺎوﻣﺘﻲ داﻳﺮهاي ﺑﺎ دو ﺷﺪت
اﻃﻼﻋﺎت ﻧﺸﺎن ﻣﻲدﻫﺪ ﻛﻪ ﺑﻴﺎن ژن، ﺑﻪﻃﻮر ﺧﻼﺻﻪ.ﻗﺮار ﻧﺪاده ﺑﺎﺷﺪ
ﺑﺮ ﺳﻄﺢ اﺑﺴﺘﺎﺗﻴﻦ ﭘﻼﺳﻤﺎ و ﻟﻨﻔﻮﺳﻴﺖ زﻧﺎن ﺟﻮان ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار
اﺑﺴﺘﺎﺗﻴﻦ ﻟﻨﻔﻮﺳﻴﺖ ﭘﺲ از ﻳﻚ ﺟﻠﺴﻪ ﺗﻤﺮﻳﻦ ﻫﻮازي اﻓﺰاﻳﺶ ﻣﻌﻨﻲداري
ﻳﻚ ﺗﻜﺮار%80 در اﻳﻦ ﺗﺤﻘﻴﻖ ﻣﻴﺰان اﺑﺴﺘﺎﺗﻴﻦ ﭘﻼﺳﻤﺎ ﺑﺎ ﺷﺪت.ﮔﺮﻓﺖ
در ﻧﻬﺎﻳﺖ ﺳﺎز و ﻛﺎر ﺗﺎﺛﻴﺮ ﺗﻤﺮﻳﻦ ﻫﻮازي ﺑﺮ ﺑﻴﺎن ژن اﺑﺴﺘﺎﺗﻴﻦ.ﻧﻤﻲﻳﺎﺑﺪ
در ﺣﺎﻟﻲ ﻛﻪ اﻳﻦ ﺗﻐﻴﻴﺮ در ﮔﺮوه،ﺑﻴﺸﻴﻨﻪ ﺑﻪﻃﻮر ﻣﻌﻨﻲداري ﻛﺎﻫﺶ ﻳﺎﻓﺖ
.ﻟﻨﻔﻮﺳﻴﺖ ﻧﻴﺎز ﺑﻪ ﺑﺮرﺳﻲﻫﺎي ﺑﻴﺸﺘﺮي دارد
ﻫﻢﭼﻨﻴﻦ ﺗﻐﻴﻴﺮات ﺳﻄﺢ اﺑﺴﺘﺎﺗﻴﻦ. ﻳﻚ ﺗﻜﺮار ﺑﻴﺸﻴﻨﻪ ﻣﻌﻨﻲدار ﻧﺒﻮد%40
1. Date Y, Nakazato M, Hashiguchi S, Dezaki K, Mondal MS, Hosoda H, et al. Ghrelin is present in pancreatic alpha-cells of humans and rats and stimulates insulin secretion. Diabetes 2002;51(1):124-9. 2. Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature 1999;402(6762):656-60. 3. St-Pierre DH, Wang L, Taché Y. Ghrelin: a novel player in the gutbrain regulation of growth hormone and energy balance. News Physiol Sci 2003;18:242-6. 4. Lagaud GJ, Young A, Acena A, Morton MF, Barrett TD, Shankley NP. Obestatin reduces food intake and suppresses body weight gain in rodents. Biochem Biophys Res Commun 2007;357(1):264-9. 5. Broglio F, Prodam F, Riganti F, Muccioli G, Ghigo E. Ghrelin: from somatotrope secretion to new perspectives in the regulation of peripheral metabolic functions. Front Horm Res 2006;35:102-14. 6. Gualillo O, Lago F, Casanueva FF, Dieguez C. One ancestor, several peptides post-translational modifications of preproghrelin generate several peptides with antithetical effects. Mol Cell Endocrinol 2006;256(1-2):1-8. 7. Zhang JV, Ren PG, Avsian-Kretchmer O, Luo CW, Rauch R, Klein C, et al. Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intake. Science 2005;310(5750):996-9. 8. Nogueiras R, Pfluger P, Tovar S, Arnold M, Mitchell S, Morris A, et al. Effects of obestatin on energy balance and growth hormone secretion in rodents. Endocrinology 2007;148(1):21-6. 9. Dun SL, Brailoiu GC, Brailoiu E, Yang J, Chang JK, Dun NJ. Distribution and biological activity of obestatin in the rat. J Endocrinol 2006;191(2):481-9.
10. Zizzari P, Longchamps R, Epelbaum J, Bluet-Pajot MT. Obestatin partially affects ghrelin stimulation of food intake and growth hormone secretion in rodents. Endocrinology 2007;148(4):1648-53. 11. Gourcerol G, Coskun T, Craft LS, Mayer JP, Heiman ML, Wang L, et al. Preproghrelin-derived peptide, obestatin, fails to influence food intake in lean or obese rodents. Obesity (Silver Spring) 2007;15(11):2643-52. 12. Unniappan S, Speck M, Kieffer TJ. Metabolic effects of chronic obestatin infusion in rats. Peptides 2008;29(8):1354-61. 13. Anderwald-Stadler M, Krebs M, Promintzer M, Mandl M, Bischof MG, Nowotny P, et al. Plasma obestatin is lower at fasting and not suppressed by insulin in insulin-resistant humans. Am J Physiol Endocrinol Metab 2007;293(5):E1393-8. 14. Guo ZF, Ren AJ, Zheng X, Qin YW, Cheng F, Zhang J, et al. Different responses of circulating ghrelin, obestatin levels to fasting, re-feeding and different food compositions, and their local expressions in rats. Peptides 2008;29(7):1247-54. 15. Sedlácková D, Dostálová I, Hainer V, Beranová L, Kvasnicková H, Hill M, et al. Simultaneous decrease of plasma obestatin and ghrelin levels after a high-carbohydrate breakfast in healthy women. Physiol Res 2008;57 Suppl 1:S29-37. 16. Reinehr T, de Sousa G, Roth CL. Obestatin and ghrelin levels in obese children and adolescents before and after reduction of overweight. Clin Endocrinol (Oxf) 2008;68(2):304-10. 17. Fontenot E, DeVente JE, Seidel ER. Obestatin and ghrelin in obese and in pregnant women. Peptides 2007;28(10):1937-44.
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1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
single session aerobic exercise ond obestatin gene expression in trained women
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23. Zwiren LD, Freedson PS, Ward A, Wilke S, Rippe JM. Estimation of VO2max: a comparative analysis of five exercise tests. Res Q Exerc Sport 1991;62(1):73-8. 24. Manshouri M, Ghanbari-Niaki A, Kraemer RR, Shemshaki A. Time course alterations of plasma obestatin and growth hormone levels in response to short-term anaerobic exercise training in college women. Appl Physiol Nutr Metab 2008;33(6):1246-9. 25. Wang J, Chen C, Wang RY. Influence of short- and long-term treadmill exercises on levels of ghrelin, obestatin and NPY in plasma and brain extraction of obese rats. Endocrine 2008;33(1):7783. 26. Saghebjoo M, Ghanbari Niaki A, Rajabi H, Hedayati M, Rahbarizadeh F. The effect of circuit exercise with different intensity on plasma and lymphocyte ghrelin and Obestatin. Iran J Endocrin Metab 2011;12(6):623-32.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
Tehran University Medical Journal;ﻫﻤﻜﺎران Vol. 69, وNo. 7, October 2011: 426-431
100
The effects of a single session aerobic exercise on obestatin gene expression in trained women
Amir Rashidlamir Ph.D.1* Mahdieh Ebrahimnia M.Sc.1 Aliakbar Hashemi Javaheri Ph.D.2 1- Department of Exercise Physiology, Faculty of Physical Education and Sport Sciences, Ferdowsi University of Mashhad, Mashhad, Iran. 2- Department of Sports Medicine, Faculty of Physical Education and Sport Sciences, Ferdowsi University of Mashhad, Mashhad, Iran.
Abstract
Received: May 04, 2011 Accepted: August 15, 2011
Background: Studies indicate that obestatin, an anti-hunger peptide, plays an important role in energy balance, GH secretion, and body weight. It has been physiologically shown that obestatin apposes the function of Ghrelin. The purpose of the present study was to investigate the effects of a single session of aerobic exercise in trained women (a 1.5-mile run) on the expression of obestatin gene found in lymphocytes. Methods: 16 trained female participants (4±1 years of training experience) were voluntarily selected from Khorasan province in Iran and were randomly divided into two groups: the control and aerobic exercise groups. The participants in the aerobic group were asked to run for 1.5 miles with a fixed speed (70 VO2 max) while the controls were passively present in the exercise environment. Following an overnight fast, blood samples (10 ml from the antecubital vein) were collected before and immediately after the exercise from all the participants. Obestatin expression was investigated after separating the lymphocytes by centrifuge and using semi-quantitative RT-PCR.
Results: There was a rise in obestatin gene expression in the case group after one session of aerobic training versus the control group but the changes were not statistically significant. Conclusion: The results indicated that a single aerobic exercise could not significantly increase the expression of obestatin. Perhaps the type, duration and intensity of the applied protocol in this study did not have a cumulative effect on this gene although these results are in harmony with the results of other studies in this regard. *
Corresponding author: Dept. of Exercise Physiology, Faculty of Physical Education and Sport Sciences, Ferdowsi University of Mashhad, Azadi Sq., Mashhad, Iran, Postal code: 9177948979 Tel: +98-511-8829580 E-mail: rashidlamir@ferdowsi.um.ac.ir
Keywords: Aerobic exercise, gene expression, lymphocyte, obestatin.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
432-437 ﻣﻬﺮاز،1390 ﺷﻤﺎره دورهﺑﻪ، 69 ﭘﺰﺷ داﻧﺸﮕﺎهﻳﻢﻋﻠﻮم ﭘﺰﺷﻜﻲ، داﻧﺸﻜ ﻓﺘﻮﺗﺮاﭘﻲ ﻗﺒﻞ 7و ،ﺑﻌﺪ زردي ﺗﻬﺮان،ﻣﺒﺘﻼ درﻜﻲﻧﻮزادان ﺗﻮﺗﺎل ﺳﺮﻣﻲ ﻣﻨﻴﺰ ﺴﻪﺪهﺳﻄﺢ ﻣﺠﻠﻪ ﻣﻘﺎﻳ
ﻣﻘﺎﻳﺴﻪ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل در ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1390/02/14 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/04/13 :
ﭼﻜﻴﺪه
ﻧﺴﺘﺮن ﺧﺴﺮوي
زﻣﻴﻨﻪ و ﻫﺪف :ﺑﻴﻠﻲروﺑﻴﻦ ﺗﻤﺎﻳﻞ ﺑﻪ ﻓﺴﻔﻮﻟﻴﭙﻴﺪﻫﺎي ﻏﺸﺎي ﺳﻠﻮﻟﻲ دارد ،از ﻣﻬﻢﺗﺮﻳﻦ آنﻫﺎ رﺳﭙﺘﻮر
*
ﻋﻠﻴﺮﺿﺎ اﻣﻴﻨﻴﺎن
Aspartate
رﺿﺎ ﺗﻘﻲﭘﻮر
N-Methyl-D-
ﻣﻲﺑﺎﺷﺪ ﻣﻨﻴﺰﻳﻢ از ﻣﻬﻢﺗﺮﻳﻦ ﻣﻬﺎرﻛﻨﻨﺪﮔﺎن اﻳﻦ رﺳﭙﺘﻮر ﻣﻲﺑﺎﺷﺪ .ﻫﺪف از اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻣﻘﺎﻳﺴﻪ ﻣﻴﺰان ﻣﻨﻴﺰﻳﻢ
ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ و ارزﻳﺎﺑﻲ روشﻫﺎي ﻧﻮﻳﻦ درﻣﺎن )ﺗﺠﻮﻳﺰ ﻣﻨﻴﺰﻳﻢ( ﻣﻲﺑﺎﺷﺪ .روش ﺑﺮرﺳﻲ :ﻣﻄﺎﻟﻌﻪ ﻧﻴﻤﻪﺗﺠﺮﺑﻲ ﮔﺮوه ﺑﻴﻤﺎريﻫﺎي ﻧﻮزادان ،ﺑﻴﻤﺎرﺳﺘﺎن ﺣﻀﺮت
)(Semi-experimental
ﻋﻠﻲ اﺻﻐﺮ )ع( ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،
ﻋﻠﻲاﺻﻐﺮ از ﻓﺮوردﻳﻦ اﻟﻲ اﺳﻔﻨﺪ 1389ﺑﻮدﻧﺪ .ﻣﻌﻴﺎرﻫﺎي ورود ﺑﻪ ﻣﻄﺎﻟﻌﻪ ﺷﺎﻣﻞ ﺳﻦ ﻛﻢﺗﺮ از 28روز ،ﻋﺪم ﻣﺎﻟﻔﻮر-
ﺗﻬﺮان ،اﻳﺮان.
و آﻳﻨﺪهﻧﮕﺮ ﻣﻲﺑﺎﺷﺪ و ﺟﻤﻌﻴﺖ ﻣﻮرد ﻣﻄﺎﻟﻌﻪ ،ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي ﺑﺴﺘﺮي در ﺑﻴﻤﺎرﺳﺘﺎن
ﻣﺎﺳﻴﻮن ،اﺧﺘﻼل ﻣﺘﺎﺑﻮﻟﻴﺴﻢ و ﺳﭙﺴﻴﺲ ،ﻋﺪم درﻳﺎﻓﺖ ﻣﻨﻴﺰﻳﻢ ﺳﻮﻟﻔﺎت در ﻣﺎدر ﺑﻮد .ﻳﺎﻓﺘﻪﻫﺎ :در ﻣﻄﺎﻟﻌﻪ 106ﻧﻮزاد زرد، 50/9درﺻﺪ ﭘﺴﺮ و 49/1درﺻﺪ دﺧﺘﺮ ﺑﻮدﻧﺪ .ﻓﺮاواﻧﻲ ﻋﻠﺖ زردي در ﺑﻴﻤﺎران ﺷﺎﻣﻞ 37ﻧﻮزاد ﺑﺎ ﻧﺎﺳﺎزﮔﺎري )(%9/34 ،ABOﭘﻨﺞ ﻧﻮزاد ﺑﺎ ﻧﺎﺳﺎزﮔﺎري ) 17 ،Rh(%7/4ﻧﻮزاد ﺑﺎ ﻣﺼﺮف ﻛﻢ ﺷﻴﺮ ﻣﺎدر ) Breast feeding (%16و 47ﻧﻮزاد ﻧﺎﺷﻲ از ﺷﻴﺮ ﻣﺎدر ) (%44/3ﺑﻮد .ﻣﻴﺎﻧﮕﻴﻦ ﻣﻨﻴﺰﻳﻢ ﻗﺒﻞ ) (2/24و ﺑﻌﺪ ) (2/12از ﻓﺘﻮﺗﺮاﭘﻲ در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ زردي ﺑﺎ اﺧﺘﻼف ﻣﻌﻨﻲدار ﻛﺎﻫﺶ ﻣﻲﻳﺎﺑﺪ ) (P<0/001و ﺑﻴﻦ دو ﺟﻨﺲ و ﺑﻴﻦ ﮔﺮوهﻫﺎي ﺳﻦ ﺑﺎرداري از ﻧﻈﺮ ﻣﻴﺎﻧﮕﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي )ﻛﻢﺗﺮ از 34ﻫﻔﺘﻪ= ،2/35ﺑﻴﻦ 35ﺗﺎ 37ﻫﻔﺘﻪ= ،2/27ﺑﻴﺶ از 38ﻫﻔﺘﻪ= (2/17و ﺑﻴﻦ ﮔﺮوهﻫﺎي وزﻧﻲ از ﻧﻈﺮ ﻣﻴﺎﻧﮕﻴﻦ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي ) 1500ﺗﺎ 2500ﮔﺮم= ،2/4ﺑﻴﺶ از 2500ﮔﺮم= (2/23و ﺑﻴﻦ ﮔﺮوهﻫﺎي ﺷﺪت ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ از ﻧﻈﺮ ﻣﻨﻴﺰﻳﻢ ﺳﺮﻣﻲ در زﻣﺎن ﺑﺴﺘﺮي )ﺧﻔﻴﻒ= ،23/2ﻣﺘﻮﺳﻂ= ،2/21ﺷﺪﻳﺪ= (2/29
*
ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﺗﻬﺮان ،ﺧﻴﺎﺑﺎن ﺷﺮﻳﻌﺘﻲ ،ﺧﻴﺎﺑﺎن ﻛﺎج،
ﺑﻴﻤﺎرﺳﺘﺎن ﺧﺎﻧﻮاده ارﺗﺶ
اﺧﺘﻼف ﻣﻌﻨﻲدار وﺟﻮد ﻧﺪارد .ﻧﺘﻴﺠﻪﮔﻴﺮي :ﻓﺘﻮﺗﺮاﭘﻲ ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ ﺑﻪ ﻛﺎﻫﺶ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل ﺳﺮﻣﻲ ﺷﻮد.
ﺗﻠﻔﻦ021-77603100 :
E-mail: dr.aminian@gmail.com
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ،ﻓﺘﻮﺗﺮاﭘﻲ ،ﻣﻨﻴﺰﻳﻢ.
ﺳﻴﺴﺘﻢ ﻋﺼﺒﻲ ﺑﺎﻋﺚ اﺧﺘﻼل در رﺷﺪ ﻋﺼﺒﻲ ،اﺧﺘﻼل ﺳﻴﻨﺎﭘﺘﻮژﻧﺰو
ﻣﻘﺪﻣﻪ
ﺗﻜﺎﻣﻞ ﻳﺎدﮔﻴﺮي -ﺧﺎﻃﺮه و ﺑﻴﻨﺎﻳﻲ ﻣﻲﮔﺮدد .ﺑﻴﻠﻲروﺑﻴﻦ ﻣﻲﺗﻮاﻧﺪ ﺑﺎﻋﺚ
رﺳﻮب ﺑﻴﻠﻲروﺑﻴﻦ ﻏﻴﺮﻛﻮﻧﮋوﮔﻪ ) (Unconjugated bilirubinﻳﺎ ﻓﺮم
ﻓﻌﺎل ﺷﺪن اﻳﻦ رﺳﭙﺘﻮر ﮔﺮدد و از اﻳﻦ ﻃﺮﻳﻖ ﺑﺎﻋﺚ آﺳﻴﺐ ﻋﺼﺒﻲ 3
اﺳﻴﺪي آن در دﻳﻮاره ﺳﻠﻮلﻫﺎي ﻋﺼﺒﻲ ﻣﻨﺠﺮ ﺑﻪ آﺳﻴﺐ داﻳﻤﻲ آنﻫﺎ
ﮔﺮدد .ﻳﻜﻲ از ﻣﻬﻢﺗﺮﻳﻦ ﻣﻬﺎرﻛﻨﻨﺪﮔﺎن رﺳﭙﺘﻮر NMDAدر اﻧﺴﺎن ﻣﻨﻴﺰﻳﻢ
ﻣﻲﮔﺮدد .ﺑﺎ در ﻧﻈﺮ ﮔﺮﻓﺘﻦ اﻳﻦ ﻣﻄﻠﺐ ﻛﻪ ﻣﻮﻟﻜﻮل ﺑﻴﻠﻲروﺑﻴﻦ ﺗﻤﺎﻳﻞ
ﻣﻲﺑﺎﺷﺪ .ﻣﻨﻴﺰﻳﻢ ﺳﻴﺴﺘﻢ ﻋﺼﺒﻲ را در ﻣﻘﺎﺑﻞ ﻫﻴﭙﻮﻛﺴﻲ ﻣﺤﺎﻓﻈﺖ ﻣﻲﻛﻨﺪ
ﺑﺎﻻﻳﻲ ﺑﺮاي اﺗﺼﺎل ﺑﻪ ﻓﺴﻔﻮﻟﻴﭙﻴﺪﻫﺎي ﻏﺸﺎ ﺳﻠﻮﻟﻲ ﭘﻼﺳﻤﺎﻳﻲ دارد،
و اﺛﺮات ﻣﺤﺎﻓﻈﺖ ﻋﺼﺒﻲ ﺧﻮد را از ﻃﺮﻳﻖ ﺑﻠﻮك ﻛﺮدن ﻣﻜﺎﻧﻴﺴﻢ NMDA
4
اﻋﻤﺎل ﻣﻲﻛﻨﺪ.
ﺑﺴﻴﺎري از اﺛﺮات
ﻣﺠﻤﻮﻋﻪ آﺳﻴﺐﻫﺎي ﻧﺎﺷﻲ از ﺑﻴﻠﻲروﺑﻴﻦ روي ﺗﻤﺎﻣﻲ آﻧﺰﻳﻢﻫﺎ و
ﺗﺤﺮﻳﻜﻲ رﺳﭙﺘﻮر
ﮔﻴﺮﻧﺪهﻫﺎي ﻋﺼﺒﻲ ﺗﺨﺮﻳﺐ اﻳﺠﺎد ﺧﻮاﻫﺪ ﻧﻤﻮد ﻛﻪ ﻳﻜﻲ از ﻣﻬﻢﺗﺮﻳﻦ
ﻓﻴﺰﻳﻮﻟﻮژﻳﻚ ﻣﻨﻴﺰﻳﻢ ﺑﺎ اﺛﺮات ﻧﻮروﺗﻮﻛﺴﻴﻚ ﺑﻴﻠﻲروﺑﻴﻦ در ﺗﻀﺎد
آنﻫﺎ رﺳﭙﺘﻮر
)(NMDA
ﻃﻮﻻﻧﻲﻣﺪت رﺳﭙﺘﻮر
2و1
N-Methyl D- Aspartateﻣﻲﺑﺎﺷﺪ.
NMDA
ﺗﺤﺮﻳﻚ
ﻣﻲﺑﺎﺷﺪ.
NMDAR
ﻛﻪ در آﺳﻔﻴﻜﺴﻲ ﭘﺮيﻧﺎﺗﺎل ﻫﻢ دﻳﺪه
ﻣﻲﺑﺎﺷﺪ.
NMDA
ﻣﻲﺷﻮد ﻣﻨﺠﺮ ﺑﻪ آﺳﻴـﺐ ﺳﻠﻮلﻫﺎي ﻣﻐﺰي ﺷﺪه و ﻋﻼوه ﺑـﺮ ﺗﻐﻴـﻴـﺮات
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻳﻚ ﻧﻮع اﺧﺘﺼﺎﺻﻲ رﺳﭙﺘﻮر ﻳﻮﻧﻴﻚ ﮔﻠﻮﺗﺎﻣﺎت
ﻧﺎم اﮔﻮﻧﻴﺴﺖ اﻧﺘﺨﺎﺑﻲ اﺳﺖ ﻛﻪ ﺑﻪ رﺳﭙﺘﻮر
NMDA
ﮔﻠﻮﺗﺎﻣﺎت ﺑﺎﻧﺪ ﻣﻲﺷﻮد وﻟﻲ ﺑﻪ دﻳﮕﺮ رﺳﭙﺘﻮرﻫﺎي ﮔﻠﻮﺗﺎﻣﺎت ﺑﺎﻧﺪ
ﻧﺴﺘﺮن ﺧﺴﺮوي و ﻫﻤﻜﺎران
NMDA
433
ﻣﻨﺠﺮ ﺑﻪ ﺑﺎز ﺷﺪن ﻛﺎﻧﺎل ﻳﻮﻧﻲ
ﻛﻪ ﺑﻪﺻﻮرت آﻳﻨﺪهﻧﮕﺮ ﺑﻮده و ﺟﻤﻌﻴﺖ ﻣﻮرد ﻣﻄﺎﻟﻌﻪ اﻳﻦ ﭘﮋوﻫﺶ ﺷﺎﻣﻞ
ﻣﻲﺷﻮد ﻛﻪ ﺑﺮاي ﻛﺎﺗﻴﻮنﻫﺎ ﻏﻴﺮ اﺧﺘﺼﺎﺻﻲ اﺳﺖ .ﻳﻚ ﺧﺎﺻﻴﺖ ﺑﻲﻧﻈﻴﺮ
ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي ﺑﻮد ﻛﻪ در ﺑﺨﺶ ﻧﻮزادان ﺑﻴﻤﺎرﺳﺘﺎن ﺣﻀﺮت
رﺳﭙﺘﻮر ،NMDAﻓﻌﺎﻟﻴﺖ واﺑﺴﺘﻪ ﺑﻪ وﻟﺘﺎژان ﻣﻲﺑﺎﺷﺪ ﻛﻪ ﺳﺒﺐ ﺑﻠﻮك
ﻋﻠﻲاﺻﻐﺮ )ع( ﺗﻬﺮان از ﻓﺮوردﻳﻦﻣﺎه ﺳﺎل 1389اﻟﻲ ﭘﺎﻳﺎن اﺳﻔﻨﺪ ﺳﺎل
ﻛﺎﻧﺎل ﻳﻮﻧﻲ ﺗﻮﺳﻂ ﻣﻨﻴﺰﻳﻢ ﺧﺎرج ﺳﻠﻮﻟﻲ ﻣﻲﺷﻮد .اﻳﻦ اﻣﺮ اﺟﺎزه ﺟﺮﻳﺎن
1389ﺑﺴﺘﺮي و ﺗﺤﺖ درﻣﺎن ﻗﺮار ﮔﺮﻓﺘﻪ ﺑﻮدﻧﺪ .اﻳﻦ ﺑﻴﻤﺎران ﺑﺮ اﺳﺎس
ﺳﺪﻳﻢ و ﻣﻘﺎدﻳﺮ ﻛﻢ ﻛﻠﺴﻴﻢ ﺑﻪ داﺧﻞ ﺳﻠﻮل و ﭘﺘﺎﺳﻴﻢ ﺑﻪ ﺧﺎرج ﺳﻠﻮل-
ﻣﻨﺤﻨﻲ ﺑﻴﻠﻲروﺑﻴﻦ ﺑﺮ ﺣﺴﺐ ﺳﻦ ﺑﻪ ﺳﺎﻋﺖ ﺗﺸﺨﻴﺺ داده ﻣﻲﺷﺪﻧﺪ و
واﺑﺴﺘﻪ ﺑﻪ وﻟﺘﺎژ را ﻣﻲدﻫﺪ .ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ ﻧﻔﻮذ ﻛﻠﺴﻴﻢ از ﻃﺮﻳﻖ
ﻫﻴﭻﻛﺪام ﻋﻼﻣﺖ دﻳﮕﺮي ﻏﻴﺮ از زردي ﻧﺪاﺷﺘﻨﺪ .ﻣﻌﻴﺎرﻫﺎي ورود ﺑﻪ
ﻳﻚ ﻧﻘﺶ ﺣﻴﺎﺗﻲ در ﭘﻼﺳﺘﻴﺴﻴﺘﻪ ﺳﻴﻨﺎﭘﺴﻲ ،ﻣﻜﺎﻧﻴﺴﻢ
ﻣﻄﺎﻟﻌﻪ ﻋﺒﺎرت ﺑﻮد از ﺳﻦ ﻛﻤﺘﺮ از ﭼﻬﺎر ﻫﻔﺘﻪ ،ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺑﺮ
ﻳﺎدﮔﻴﺮي و ﺣﺎﻓﻈﻪ دارد .رﺳﭙﺘﻮر NMDAاز دو ﻧﻈﺮ ﻣﺘﻔﺎوت اﺳﺖ :اول،
اﺳﺎس ﻧﺘﻴﺠﻪ ﺑﻴﻠﻲروﺑﻴﻦ و ﺑﺮ اﺳﺎس ﻣﻨﺤﻨﻲ ﺑﻴﻠﻲروﺑﻴﻦ ﺑﺮ ﺣﺴﺐ ﺳﻦ
ﻧﻤﻲﺷﻮد .ﻓﻌﺎﻟﻴﺖ رﺳﭙﺘﻮرﻫﺎي
NMDARs
ﻫﻢ دروازه ﻟﻴﮕﺎﻧﺪي Ligand-gateو ﻫﻢ واﺑﺴﺘﻪ ﺑﻪ وﻟﺘﺎژ اﺳﺖ دوم
ﺑﻪ ﺳﺎﻋﺖ ﻛﻪ ﺑﺎﻻﺗﺮ از ﺣﺪ ﻣﺠﺎز ﺑﺮاي آن ﻧﻮزاد ﺑﺎﺷﺪ ،ﻋﺪم وﺟﻮد
5
اﺧﺘﻼﻻت ﻣﺘﺎﺑﻮﻟﻴﺴﻢ ﻣﺎدرزادي ،ﻋﺪم ﺷﻮاﻫﺪ ﺳﭙﺴﻴﺲ ﻧﻮزادي در ﻣﻌﺎﻳﻨﻪ
ﻳﻚ ﻛﺎﻧﺎل ﻳﻮﻧﻲ ﻏﻴﺮ اﺧﺘﺼﺎﺻﻲ ﻛﺎﺗﻴﻮﻧﻲ اﺳﺖ ﻛﻪ
ﺷﺎﻣﻞ ﺗﺐ ،اﺧﺘﻼل ﺗﻐﺬﻳﻪ ،ﻛﺎﻫﺶ رﻓﻠﻜﺲﻫﺎي ﻧﻮزادي ،ﻋﺪم درﻳﺎﻓﺖ
اﺟﺎزه ﻋﺒﻮر ﻛﻠﺴﻴﻢ ،ﺳﺪﻳﻢ و ﭘﺘﺎﺳﻴﻢ ﺑﻪ داﺧﻞ ﺳﻠﻮل را ﻣﻲدﻫﺪ .ﭘﺘﺎﻧﺴﻴﻞ
ﺳﻮﻟﻔﺎت ﻣﻨﻴﺰﻳﻢ در ﻣﺎدر .ﻧﻮزادان ﺑﺴﺘﺮي داراي ﻣﻌﻴﺎرﻫﺎي ورود ﺑﻪ
)Excitatory Postsynaptic Potential (EPSP
ﻣﻄﺎﻟﻌﻪ ﺑﻪﺻﻮرت ﻧﻤﻮﻧﻪﮔﻴﺮي ﭘﻲدرﭘﻲ Consecutiveوارد ﻣﻄﺎﻟﻌﻪ
ﻏﻠﻈﺖ ﻛﻠﺴﻴﻢ داﺧﻞ ﺳﻠﻮﻟﻲ را اﻓﺰاﻳﺶ
ﺷﺪﻧﺪ .اﻃﻼﻋﺎت دﻣﻮﮔﺮاﻓﻴﻚ ﺷﺎﻣﻞ ﺟﻨﺲ ،ﺳﻦ ﺣﺎﻣﻠﮕﻲ ،ﺳﻦ ﻧﻮزاد در
ﻣﻲدﻫﺪ .ﻛﻠﺴﻴﻢ ﺑﻪﻋﻨﻮان ﭘﻴﺎﻣﺒﺮ ﺛﺎﻧﻮﻳﻪ در راهﻫﺎي ﺳﻴﮕﻨﺎلدﻫﻨﺪه ﻣﺨﺘﻠﻔﻲ
ﺷﺮوع زردي ،ﻃﻮل ﻣﺪت زردي ،وزن ﻧﻮزاد در زﻣﺎن ﺑﺴﺘﺮي از واﻟﺪﻳﻦ
ﺗﻮﺳﻂ ﻣﻨﻴﺰﻳﻢ در
ﺑﻴﻤﺎر ﻛﺴﺐ و در ﭘﺮﺳﺶﻧﺎﻣﻪ ﺛﺒﺖ ﺷﺪ .ﻣﻴﺰان ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺑﺮ
ﺳﻄﻮح ﻓﻴﺰﻳﻮﻟﻮژﻳﻚ ﺑﻠﻮك ﻣﻲﺷﻮد .ﺑﺮاي ﻛﺎﻧﺎل ﺑﻠﻮكﻧﺸﺪه ،ﺳﻠﻮل
اﺳﺎس اوﻟﻴﻦ آزﻣﺎﻳﺶ ﺑﻴﻠﻲروﺑﻴﻦ اﺧﺬ ﺷﺪه از ﻧﻮزاد و ﺳﺎﻳﺮ آزﻣﺎﻳﺸﺎت
ﭘﺴﺖ ﺳﻴﻨﺎﭘﺴﻲ ﺑﺎﻳﺪ دﭘﻼرﻳﺰه ﺑﺎﺷﺪ 5.ﺑﺪون در ﻧﻈﺮ ﮔﺮﻓﺘﻦ ﻋﻠﺖ ،ﻫﺪف
ﻏﺮﺑﺎلﮔﺮي ﺷﺎﻣﻞ ،CBCاﺳﻤﻴﺮ ﺧﻮن ﻣﺤﻴﻄﻲ ،ﮔﺮوه ﺧﻮﻧﻲ و ،Rh
از درﻣﺎن ﺟﻠﻮﮔﻴﺮي از رﺳﻴﺪن ﺑﻴﻠﻲروﺑﻴﻦ ﻏﻴﺮ ﻣﺴﺘﻘﻴﻢ ﺑﻪﻣﻘﺎدﻳﺮ
G6PD ،D-Coombs
و Reticﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار ﮔﺮﻓﺖ .ﺷﺪت زردي
ﻧﻮروﺗﻮﻛﺴﻴﻚ ﻣﻲﺑﺎﺷﺪ .ﺑﺎ ﻓﺘﻮﺗﺮاﭘﻲ و در ﺻﻮرت ﻋﺪم ﭘﺎﺳﺦ ﺑﺎ ﺗﻌﻮﻳﺾ
ﺑﺮ اﺳﺎس ﻣﻴﺰان ﺑﻴﻠﻲروﺑﻴﻦ ﺗﻮﺗﺎل در ﻧﻮزادان ﺗﺮم ﺗﻘﺴﻴﻢﺑﻨﺪي ﺷﺪ
ﺧﻮن ﻣﻴﺰان ﺑﻴﻠﻲروﺑﻴﻦ را ﺑﻪ ﻣﻘﺎدﻳﺮ ﭘﺎﻳﻴﻦﺗﺮ از ﺣﺪ ﺗﻌﻴﻴﻦﺷﺪه
)ﺧﻔﻴﻒ :ﺑﻴﻦ 15ﺗﺎ ،18ﻣﺘﻮﺳﻂ :ﺑﻴﻦ 18ﺗﺎ ،20ﺷﺪﻳﺪ 20 :ﺑﻪ ﺑﺎﻻ( .از
ﻣﻲرﺳﺎﻧﻴﻢ ﺗﺎ از اﺛﺮات ﻧﻮروﺗﻮﻛﺴﻴﻚ ﺑﻴﻠﻲروﺑﻴﻦ ﺟﻠﻮﮔﻴﺮي ﻧﻤﺎﻳﻴﻢ.
ﺗﻤﺎﻣﻲ ﺷﺮﻛﺖﻛﻨﻨﺪﮔﺎن در ﻣﻄﺎﻟﻌﻪ ﻳﻚ ﻧﻤﻮﻧﻪ ﻣﻨﻴﺰﻳﻢ ﻗﺒﻞ از ﻓﺘﻮﺗﺮاﭘﻲ و
اﻳﻦﻛﻪ ﻧﻴﺎزﻣﻨﺪ ﻓﻌﺎل ﺷﺪن ﺑﺎ دو ﻟﻴﮕﺎﻧﺪ ﮔﻠﻮﺗﺎﻣﺎت و ﮔﻠﻴﺴﻴﻦ اﺳﺖ. رﺳﭙﺘﻮر
NMDA
ﺗﺤﺮﻳﻜﻲ ﭘﺴﺖ ﺳﻴﻨﺎﭘﺴﻲ ﺑﺎ ﻓﻌﺎﻟﻴﺖ رﺳﭙﺘﻮر
NMDA
ﻋﻤﻞ ﻣﻲﻛﻨﺪ .اﮔﺮﭼﻪ ﻛﺎﻧﺎل ﻛﺎﺗﻴﻮﻧﻲ رﺳﭙﺘﻮر
NMDA
از آﻧﺠﺎﻳﻲﻛﻪ ﻣﻴﺰان ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل در ﺑﺪن ﻧﻮزادان و ارﺗﺒﺎط آن ﺑﺎ
ﻳﻚ ﻧﻤﻮﻧﻪ ﭘﺲ از ﻓﺘﻮﺗﺮاﭘﻲ اﺧﺬ ﺷﺪ .ﻧﻤﻮﻧﻪﮔﻴﺮي ﻣﻨﻴﺰﻳﻢ ﻫﻢزﻣﺎن ﺑﺎ
ﺳﻄﺢ ﺑﻴﻠﻲروﺑﻴﻦ ،در ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ دوران ﻧﻮزادي ﺑﺮرﺳﻲ ﻛﺎﻓﻲ
اﻧﺠﺎم ﺗﺴﺖﻫﺎي ﻻزم در ﻣﻮرد زردي ﻧﻮزادي اﻧﺠﺎم و ﺑﺎﺑﺖ اﻳﻦ ﻣﺴﺎﻟﻪ
ﻧﺸﺪه ،در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل در ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻧﻮزادي
ﺧﻮنﮔﻴﺮي اﺿﺎﻓﻪ اﻧﺠﺎم ﻧﺸﺪ .ﻣﺠﺪدا ﭘﺲ از 24ﺳﺎﻋﺖ از ﺷﺮوع
ﺗﻌﻴﻴﻦ ﻣﻲﺷﻮد .ﺑﺎ ﻓﺮض اﺛﺮات ﻣﺤﺎﻓﻈﺘﻲ ﻣﻨﻴﺰﻳﻢ در ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ
ﻓﺘﻮﺗﺮاﭘﻲ ﺑﻴﻠﻲروﺑﻴﻦ و ﻣﻨﻴﺰﻳﻢ ﺑﺮرﺳﻲ ﺷﺪ .زﻣﺎن ﺗﺮﺧﻴﺺ ﻧﻮزادان ﺑﺮ
ﻧﻮزادي ،ﻣﻴﺰان ﻣﻨﻴﺰﻳﻢ را در ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ ﻣﻘﺎﻳﺴﻪ و ﺗﺎﺛﻴﺮ
اﺳﺎس آزﻣﺎﻳﺶ ﺳﻄﺢ ﺑﻴﻠﻲروﺑﻴﻦ ﺳﺮم و رﺳﻴﺪن ﺑﻪ ﻣﻨﻄﻘﻪ ﺑﺎ ﺧﻄﺮ ﭘﺎﻳﻴﻦ
درﻣﺎﻧﻲ آن ﺑﺮرﺳﻲ ﻣﻲﺷﻮد .ﻫﻢﭼﻨﻴﻦ ارﺗﺒﺎط ﺑﻴﻦ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل و
ﻣﻨﺤﻨﻲ ﺳﻄﺢ ﺑﻴﻠﻲروﺑﻴﻦ ﺳﺮم ﺑﺮ ﺣﺴﺐ ﺳﺎﻋﺖ ﭘﺲ از ﺗﻮﻟﺪ ﺑﻮده اﺳﺖ.
ﺷﺪت ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺑﺮرﺳﻲ ﻣﻲﺷﻮد ﺑﺪﻳﻦﺗﺮﺗﻴﺐ ﻧﻮزادان در
ﺑﻌﺪ از ﺟﻤﻊآوري اﻃﻼﻋﺎت در ﭘﺮﺳﺶﻧﺎﻣﻪ و ورود ﺑﻪ ﻧﺮماﻓﺰار آﻣﺎري 2
ﻣﻌﺮض ﺧﻄﺮ ﺷﻨﺎﺳﺎﻳﻲ و زﻣﺎن ﺗﺮﺧﻴﺺ ﻣﻨﺎﺳﺐ و روشﻫﺎي ﻧﻮﻳﻦ
SPSSوﻳﺮاﺳﺖ 17ﺑﺎ روشﻫﺎي ،Student’s t-testو ﺳﺎﻳﺮ روشﻫﺎ
درﻣﺎن )ﺗﺠﻮﻳﺰ ﻣﻨﻴﺰﻳﻢ( ارزﻳﺎﺑﻲ ﻣﻲﺷﻮد.
ﺑﺮ ﺣﺴﺐ ﻧﻴﺎز اﻃﻼﻋﺎت ﺗﺤﻠﻴﻞ ﺷﺪ .ﺳﻄﺢ ﻣﻌﻨﻲدار در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻛﻢﺗﺮ از 0/05ﺑﻮد .ﻣﺮاﺣﻞ ﺗﺤﻘﻴﻖ ﺑﺮ اﺳﺎس ﺣﻔﻆ اﺳﺮار ﺑﻴﻤﺎران و ﺑﺮ
روش ﺑﺮرﺳﻲ
اﺳﺎس ﻗﻄﻊﻧﺎﻣﻪ ﻫﻠﺴﻴﻨﻜﻲ اﻧﺠﺎم و در ﻛﻤﻴﺘﻪ اﺧﻼق ﺑﻴﻤﺎرﺳﺘﺎن ﺑﻪ ﺗﺎﻳﻴﺪ
ﻣﻄﺎﻟﻌﻪ اﻧﺠﺎمﺷﺪه از ﻧﻮع ﻧﻴﻤﻪﺗﺠﺮﺑﻲ ) (Semi experimentalﻣﻲﺑﺎﺷﺪ
رﺳﻴﺪه اﺳﺖ.
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
434
ﻣﻘﺎﻳﺴﻪ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل در ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ
ﺟﺪول :1-وﻳﮋﮔﻲﻫﺎي ﻣﺮﺗﺒﻂ ﺑﺎ زردي در ﺑﻴﻤﺎران ﻣﻴﺎﻧﮕﻴﻦ )ﻣﻴﺎﻧﻪ(
اﻧﺤﺮافﻣﻌﻴﺎر
وﻳﮋﮔﻲ
ﻓﺮاواﻧﻲ
درﺻﺪ در ﮔﺮوه
وﻳﮋﮔﻲ ﺳﻦ ﺷﺮوع زردي )روز(
(3) 3/16
1/736
اﺳﻤﻴﺮ ﺧﻮن ﻣﺤﻴﻄﻲ ﻏﻴﺮ ﻃﺒﻴﻌﻲ
0
0
ﺳﻦ ﭘﺎﻳﺎن زردي )روز(
(7) 7/55
2/948
9
8/5
دوره زﻣﺎﻧﻲ ﻓﺘﻮﺗﺮاﭘﻲ )روز(
(4) 4/36
2/627
2
1/9
18/29
3/619
ABO
37
34/9
14/83
2/534
Rh
5
4/7
ﻫﻤﺎﺗﻮﻛﺮﻳﺖ )(%
44/34
6/869
ﻣﺼﺮف ﻛﻢ ﺷﻴﺮ ﻣﺎدر Breast feeding
17
16
رﺗﻴﻜﻮﻟﻮﺳﻴﺖ )(%
2/29
2/297
ﺷﻴﺮ ﻣﺎدر Breast milk
47
44/3
ﺑﻴﻠﻲروﺑﻴﻦ ﺗﻮﺗﺎل ﻫﻤﻮﮔﻠﻮﺑﻴﻦ
)(mg/dl
)(gr/dl
ﻛﻤﺒﻮد
ﻛﻮﻣﺒﺲ ﻣﺴﺘﻘﻴﻢ ﻣﺜﺒﺖ ﻧﺎﺳﺎزﮔﺎري
ﻧﺎﺳﺎزﮔﺎري
ﺟﺪول :2-ﻣﻨﻴﺰﻳﻢ و ﺑﻴﻠﻲروﺑﻴﻦ ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ در ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي وﻳﮋﮔﻲ
ﻗﺒﻞ از ﻓﺘﻮﺗﺮاﭘﻲ
ﭘﺲ از ﻓﺘﻮﺗﺮاﭘﻲ
t-test
P
ﻣﻴﺎﻧﮕﻴﻦ ﻣﻨﻴﺰﻳﻢ
(0/270) 2/24
(0/231) 2/12
6/332
*0/001
)اﻧﺤﺮافﻣﻌﻴﺎر( ﻣﻴﺎﻧﮕﻴﻦ ﺑﻴﻠﻲروﺑﻴﻦ
(3/619) 18/29
(3/622) 9/15
25/984
ﺟﺪول :3-ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي ﺑﻪدﻟﻴﻞ زردي )ﺳﻦ ﺑﺎرداري و وزن ﺗﻮﻟﺪ(
ﻣﺘﻐﻴﺮ
ﺗﻘﺴﻴﻢﺑﻨﺪي
ﺟﻨﺲ
ﭘﺴﺮ
ﻣﻴﺎﻧﮕﻴﻦ ﻣﻨﻴﺰﻳﻢ 2/28
0/275
دﺧﺘﺮ
2/19
0/259
ﻛﻢﺗﺮ از 34ﻫﻔﺘﻪ
2/35
0/264
35ﺗﺎ 37ﻫﻔﺘﻪ
2/27
0/284
ﺑﻴﺶ از 38ﻫﻔﺘﻪ
2/17
0/236
ﻛﻢﺗﺮ از 1500gr
0
0
1500-2500 gr
2/4
0/200
ﺑﻴﺶ از 2500gr
2/23
0/272
ﺧﻔﻴﻒ )(15-18
2/23
0/290
ﻣﺘﻮﺳﻂ )(18-20
2/21
0/250
ﺷﺪﻳﺪ )ﺑﻴﺶ از (20
2/29
0/238
**0/001 ﺳﻦ ﺑﺎرداري
)اﻧﺤﺮافﻣﻌﻴﺎر( * P<0/001و t-test=6/332
G6PD
** P<0/001و t-test=25/984
وزن ﺗﻮﻟﺪ
ﻳﺎﻓﺘﻪﻫﺎ در ﻣﻄﺎﻟﻌﻪ اﻧﺠﺎمﺷﺪه ﺑﺮ روي 106ﺑﻴﻤﺎر ﺑﺎ ﺗﺸﺨﻴﺺ زردي ،ﻣﻴﺎﻧﮕﻴﻦ ﺳﻦ ﺑﺎرداري 37/34±1/286ﻫﻔﺘﻪ )ﺣﺪاﻗﻞ= ،33ﺣﺪاﻛﺜﺮ= (41و ﻣﻴﺎﻧﮕﻴﻦ وزن زﻣﺎن ﺗﻮﻟﺪ 3172/12±436/936ﮔﺮم )ﺣﺪاﻗﻞ= ،2022
ﺷﺪت زردي
* P=0/078و t-test=1/783
اﻧﺤﺮافﻣﻌﻴﺎر
** P=0/122و F=2/147
*P
*0/078
**0/122
***0/113
0/558
*** P=0/113و t-test=1/1597
ﺣﺪاﻛﺜﺮ= (4300ﺑﻮد 50/9 .درﺻﺪ ﭘﺴﺮ و 49/1درﺻﺪ دﺧﺘﺮ ﺑﻮدﻧﺪ. وﻳﮋﮔﻲﻫﺎي ﻣﺮﺗﺒﻂ ﺑﺎ زردي ﻧﻮزادان در ﺟﺪول 1ﺧﻼﺻﻪ ﺷﺪهاﻧﺪ .در ﺿﻤﻦ در 93/4ﻧﻮزادان ﻓﻘﻂ ﻓﺘﻮﺗﺮاﭘﻲ و در 6/6درﺻﺪ ﻋﻼوه ﺑﺮ
زﻣﺎن ﺑﺴﺘﺮي اﺧﺘﻼف ﻣﻌﻨﻲدار وﺟﻮد ﻧﺪارد ) F=2/147و .(P=0/122ﺑﺎ
ﻓﺘﻮﺗﺮاﭘﻲ ،ﺗﻌﻮﻳﺾ ﺧﻮن ﻧﻴﺰ اﻧﺠﺎم ﺷﺪه ﺑﻮد .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺟﺪول 2و ﺑﺮ
ﺗﻮﺟﻪ ﺑﻪ ﺟﺪول 2و ﺑﺎ ﻋﻨﺎﻳﺖ ﺑﻪ اﻳﻦﻛﻪ ﻳﻜﻲ از ﮔﺮوهﻫﺎي وزﻧﻲ )ﻛﻢﺗﺮ
اﺳﺎس ﻧﺘﺎﻳﺞ ﺗﺴﺖ Paired samples t-testﻣﻴﺎﻧﮕﻴﻦ ﻣﻨﻴﺰﻳﻢ ﻗﺒﻞ و ﺑﻌﺪ
از 1500ﮔﺮم( ﻣﻘﺪار ﻋﺪدي ﺻﻔﺮ دارد ﺑﻪﺟﺎي ﺗﺴﺖ
ANOVA
از
Student’s t-test
از ﻓﺘﻮﺗﺮاﭘﻲ در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ زردي ﺑﺎ اﺧﺘﻼف ﻣﻌﻨﻲدار ﻛﺎﻫﺶ
Student’s t-testاﺳﺘﻔﺎده ﻛﺮدﻳﻢ و ﺑﺮ اﺳﺎس ﻧﺘﺎﻳﺞ
ﻣﻲﻳﺎﺑﺪ .ﻫﻢﭼﻨﻴﻦ ﺑﺮ اﺳﺎس ﻧﺘﺎﻳﺞ Paired samples t-testﻣﻴﺎﻧﮕﻴﻦ
ﺑﻴﻦ ﮔﺮوهﻫﺎي وزﻧﻲ زﻣﺎن ﺗﻮﻟﺪ از ﻧﻈﺮ ﻣﻴﺎﻧﮕﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ در
ﺑﻴﻠﻲروﺑﻴﻦ ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ ﻧﻴﺰ در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ زردي ﺑﺎ
زﻣﺎن ﺑﺴﺘﺮي اﺧﺘﻼف ﻣﻌﻨﻲدار وﺟﻮد ﻧﺪارد ) T=1/1597و .(P=0/113
اﺧﺘﻼف ﻣﻌﻨﻲدار ﻛﺎﻫﺶ ﻣﻲﻳﺎﺑﺪ .ﺑﺮ اﺳﺎس ﻧﺘﺎﻳﺞ Student’s t-testﺑﻴﻦ
ﺑﻪﻋﻼوه ﺑﺮ اﺳﺎس ﻧﺘﺎﻳﺞ ﺗﺴﺖ
دو ﺟﻨﺲ )ﭘﺴﺮ= ،2/28±0/275دﺧﺘﺮ= (2/19±0/259از ﻧﻈﺮ ﻣﻴﺎﻧﮕﻴﻦ
ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ از ﻧﻈﺮ ﻣﻴﺎﻧﮕﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي
ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي اﺧﺘﻼف ﻣﻌﻨﻲدار وﺟﻮد ﻧﺪارد
و .(P=0/558ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ
) t-test=1/783و .(P=0/078ﻫﻢﭼﻨﻴﻦ ﺑﺮ اﺳﺎس ﻧﺘﺎﻳﺞ ﺗﺴﺖ
اﺧﺘﻼف ﻣﻌﻨﻲدار وﺟﻮد ﻧﺪارد
ANOVA
)F=0/586
ﺑﻴﻦ ﮔﺮوهﻫﺎي ﺷﺪت
ANOVA
ﻧﺘﺎﻳﺞ Student’s t-testﺑﻴﻦ دو ﮔﺮوه داراي ﻟﻴﺰ )رﺗﻴﻜﻮﻟﻮﺳﻴﺖ ﺑﻴﺶ از
ﺑﻴـﻦ ﮔﺮوهﻫﺎي ﺳﻦ ﺑﺎرداري از ﻧﻈﺮ ﻣﻴـﺎﻧﮕﻴـﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴـﺰﻳﻢ در
ﭘﻨﺞ( و ﻓﺎﻗﺪ ﻟﻴﺰ )داراي ﻟﻴﺰ= ،2/19±0/253ﻓﺎﻗﺪ ﻟﻴﺰ= (2/25±0/273
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﻧﺴﺘﺮن ﺧﺴﺮوي و ﻫﻤﻜﺎران
435
از ﻧﻈﺮ ﻣﻴﺎﻧﮕﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي اﺧﺘﻼف ﻣﻌﻨﻲدار
داد ﻛﻪ ﻏﻠﻈﺖ ﭘﺎﻳﻴﻦﺗﺮ ﺳﺮﻣﻲ و ﺑﻨﺪ ﻧﺎف روي و ﻣﻨﻴﺰﻳﻢ ﻫﻢ در ﻧﻮزادان
وﺟﻮد ﻧﺪارد ) T= -0/702و .(P=0/484
ﺑﺎ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻣﺘﻮﺳﻂ و ﻫﻢ در ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺷﺪﻳﺪ ﻛﻪ ﺗﺤﺖ درﻣﺎن ﺗﻌﻮﻳﺾ ﺧﻮن ﻗﺮار ﮔﺮﻓﺘﻨﺪ در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﻧﻮزادان ﺑﺪون
ﺑﺤﺚ
ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ وﺟﻮد دارد ،آنﻫﺎ ﻧﺘﻴﺠﻪ ﮔﺮﻓﺘﻨﺪ ﻛﻪ ﺳﻮءﺗﻐﺬﻳﻪ ﻣﺎدر
ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﺑﺮاي ﺗﻌﻴﻴﻦ ارﺗﺒﺎط ﺑﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل در
در زﻣﺎن ﺑﺎرداري ﻣﻨﺠﺮ ﺑﻪ ﻫﻴﭙﻮﻣﻨﻴﺰﻳﻤﻲ ﻧﻮزادي و ﻣﺎدري ﻣﻲﮔﺮدد ﻛﻪ ﺑﺎ
ﻧﻮزادان ﻣﺒﺘﻼ ﺑﻪ زردي ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲ ﺑﻮد ﻛﻪ ﻣﺸﺨﺺ ﺷﺪ در
اﺛﺮ ﻣﻌﻜﻮس ﻧﺎﺷﻲ از آﻧﺰﻳﻢﻫﺎ ﺑﺮ ﻣﺘﺎﺑﻮﻟﻴﺴﻢ ﺑﻴﻠﻲروﺑﻴﻦ و آﻧﺰﻳﻢﻫﺎي
ﺑﻴﻤﺎران ﺑﺎ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ،اﻓﺰاﻳﺶ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﻧﻴﺰ دارﻳﻢ و ﺳﻄﺢ
آﻧﺘﻲاﻛﺴﻴﺪاﻧﺖ ﺑﺮ ارﻳﺘﺮوﺳﻴﺖﻫﺎ ﺑﺎﻋﺚ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻏﻴﺮ ﻣﺴﺘﻘﻴﻢ 6
ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل ﺳﺮﻣﻲ ﭘﺲ از ﻓﺘﻮﺗﺮاﭘﻲ ﻛﺎﻫﺶ ﻣﻌﻨﻲدار ﭘﻴﺪا ﻣﻲﻛﻨﺪ
ﻣﻲﮔﺮدد .در ﻣﻄﺎﻟﻌﻪ دﻳﮕﺮ ،Misraارﺗﺒﺎط ﺑﻴﻦ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ و ﻣﻮاد
) (t-test=6/332و ) .(P<0/001ﺳﻌﻲ ﺑﺮ اﻳﻦ ﺑﻮد ﻛﻪ در اﻳﻦ ﻣﻄﺎﻟﻌﻪ
ﻣﻌﺪﻧﻲ ﻣﺨﺘﻠﻒ ﻣﻮرد ارزﻳﺎﺑﻲ ﻗﺮار ﮔﺮﻓﺖ و ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل
ارﺗﺒﺎط ﺑﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ در زﻣﺎن ﺑﺴﺘﺮي ﺑﺎ ﺟﻨﺲ ،ﺳﻦ ﺑﺎرداري
ﻣﺸﺨﺼﺎ در 30ﻧﻮزاد ﺑﺎ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻫﻤﻮﻟﻴﺘﻴﻚ در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﮔﺮوه 7
)ﻛﻢﺗﺮ از 34ﻫﻔﺘﻪ 35 ،ﺗﺎ 37ﻫﻔﺘﻪ ،ﺑﻴﺶﺗﺮ از 38ﻫﻔﺘﻪ( ،وزن ﺗﻮﻟﺪ
ﻛﻨﺘﺮل ﭘﺎﻳﻴﻦﺗﺮ ﺑﻮد Pintov .ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل ،ﻣﺲ و روي ﺑﻨﺪ ﻧﺎف
)ﻛﻢﺗﺮ از 1500ﮔﺮم 1500 ،ﺗﺎ 2500ﮔﺮم ،ﺑﻴﺶﺗﺮ از 2500ﮔﺮم(
را ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار داد ﺗﺎ اﺣﺘﻤﺎل ﺑﺮوز ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ را در ﻃﻲ
ﺗﻌﻴﻴﻦ ﮔﺮدﻳﺪ ﻛﻪ در ﻫﻴﭻﻛﺪام از ﻣﻮارد ﻓﻮق ارﺗﺒﺎط ﻣﻌﻨﻲداري ﺑﻪدﺳﺖ
48ﺳﺎﻋﺖ آﻳﻨﺪه ﭘﻴﺶﺑﻴﻨﻲ ﻛﻨﺪ ﻛﻪ ﻫﻴﭻﮔﻮﻧﻪ ﺗﻔﺎوت ﻣﻌﻨﻲداري در ﻣﻮرد
ﻧﻴﺎﻣﺪ .ﻫﻢﭼﻨﻴﻦ در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﺑﻴﻦ ﺷﺪت ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ و ﺳﻄﺢ
اﻳﻦ ﻣﻮاد ﻣﻌﺪﻧﻲ در ﺑﻴﻦ ﻧﻮزاداﻧﻲ ﺑﺎ و ﺑﺪون ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﭘﻴﺪا 8
ﻣﻨﻴﺰﻳﻢ ﭘﻼﺳﻤﺎ ارﺗﺒﺎط ﻣﻌﻨﻲداري ﺑﻪدﺳﺖ ﻧﻴﺎﻣﺪ اﻟﺒﺘﻪ ﺷﺎﻳﺪ ﻋﻠﺖ اﻳﻦ اﻣﺮ
ﻧﻜﺮد .از ﻃﺮف دﻳﮕﺮ در ﻣﻄﺎﻟﻌﻪ Sariciارﺗﺒﺎط ﻣﺜﺒﺘﻲ ﺑﻴﻦ ﺳﻄﺢ
ﺗﺎﺧﻴﺮ در ﺧﻮنﮔﻴﺮي ﺑﺎﺑﺖ ﻣﻨﻴﺰﻳﻢ ﺑﻪدﻟﻴﻞ رﻋﺎﻳﺖ ﻣﺴﺎﻳﻞ اﺧﻼﻗﻲ ﺑﺎﺷﺪ.
ﺑﻴﻠﻲروﺑﻴﻦ ﺳﺮم و ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﻳﻮﻧﻴﺰه ﭘﻼﺳﻤﺎ وﺟﻮد داﺷﺖ؛ در ﮔﺮوه
)در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻫﻴﭻ ﺧﻮنﮔﻴﺮي از ﻧﻮزاد ﺻﺮﻓﺎ ﺑﺮاي اﻧﺠﺎم ﺗﺤﻘﻴﻖ
ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺷﺪﻳﺪ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﻳﻮﻧﻴﺰه ﺳﺮم ﺑﻪﻃﻮر ﻣﻌﻨﻲداري در
ﺑﻪﻋﻤﻞ ﻧﻴﺎﻣﺪ و ﺗﻤﺎﻣﻲ ﻣﻮارد ارزﻳﺎﺑﻲﻫﺎي آزﻣﺎﻳﺸﮕﺎﻫﻲ ﻫﻤﺮاه
ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﮔﺮوه ﻣﺘﻮﺳﻂ ﺑﺎﻻﺗﺮ ﺑﻮد .ﻫﻢﭼﻨﻴﻦ در ﮔﺮوه ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ
ﺧﻮنﮔﻴﺮيﻫﺎي ﻻزم دﻳﮕﺮ ﺟﻬﺖ ﺗﺸﺨﻴﺺ و درﻣﺎن زردي ﻧﻮزاد اﻧﺠﺎم
ﺷﺪﻳﺪ ،ارﺗﺒﺎط آﻣﺎري ﻣﺜﺒﺖ ﺑﻴﻦ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ ﻳﻮﻧﻴﺰه و ﺷﺪت
ﺷﺪ ﺑﻪﻫﻤﻴﻦ دﻟﻴﻞ ﻧﻮزاداﻧﻲ ﻛﻪ ﺑﺎ ﺑﺮﮔﻪ آزﻣﺎﻳﺶ از ﺳﺎﻳﺮ ﻣﺮاﻛﺰ ﻳﺎ
ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ وﺟﻮد داﺷﺖ و ﻧﺘﻴﺠﻪ ﮔﺮﻓﺖ ﻛﻪ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﻳﻮﻧﻴﺰه 9
ﻣﻄﺐﻫﺎ ارﺟﺎع ﻣﻲﺷﺪﻧﺪ ،ﭘﺲ از ﮔﺬﺷﺖ ﺷﺶ ﺳﺎﻋﺖ از ﻓﺘﻮﺗﺮاﭘﻲ ﺑﺎ
ﭘﻼﺳﻤﺎ ﺑﺎ اﻓﺰاﻳﺶ ﺳﻄﺢ ﺑﻴﻠﻲروﺑﻴﻦ ﺳﺮم اﻓﺰاﻳﺶ ﻣﻲﻳﺎﺑﺪ .در ﻣﻄﺎﻟﻌﻪ ﻣﺎ
ﺳﺎﻳﺮ آزﻣﺎﻳﺸﺎﺗﺸﺎن ﺑﺮرﺳﻲ ﻣﻨﻴﺰﻳﻢ ﻧﻴﺰ ﺻﻮرت ﮔﺮﻓﺖ .ﻫﺮﭼﻨﺪ اﺛﺮات
ﻧﻴﺰ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﺳﺮﻣﻲ در ﻣﻮارد ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺑﺎ درﻣﺎن ﻛﺎﻫﺶ
ﺑﻪﺧﻮﺑﻲ
ﻳﺎﻓﺖ ﻛﻪ ﺷﺎﻳﺪ ﺑﻪﻋﻠﺖ اﻓﺰاﻳﺶ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﭘﻼﺳﻤﺎ ﻫﻢزﻣﺎن ﺑﺎ
ﺗﻮﺻﻴﻒ و ﺑﺮرﺳﻲ ﺷﺪه اﺳﺖ و ﻧﻘﺶ آن و اﺛﺮات ﻧﻮروﭘﺮوﺗﻜﺘﻴﻮ آن در
ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺑﺎﺷﺪ ﻛﻪ ﭘﺲ از ﻛﺎﻫﺶ ﺳﻄﺢ ﺑﻴﻠﻲروﺑﻴﻦ ،ﺳﻄﺢ
ﭘﺎﺗﻮﻓﻴﺰﻳﻮﻟﻮژي آﻧﺴﻔﺎﻟﻮﭘﺎﺗﻲ ﻫﻴﭙﻮﻛﺴﻴﻚ اﻳﺴﻜﻤﻴﻚ ﻣﺸﺨﺺ ﺷﺪه اﺳﺖ
ﻣﻨﻴﺰﻳﻢ ﻧﻴﺰ ﻛﺎﻫﺶ ﻣﻲﻳﺎﺑﺪ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ ﺗﻨﻬﺎ %1ﻣﻨﻴﺰﻳﻢ ﺑﺪن ﺧﺎرج
وﻟﻲ ارﺗﺒﺎط ﺑﻴﻦ ﻣﻨﻴﺰﻳﻢ و ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻧﻮزادي ﻫﻨﻮز ﺑﻪﻃﻮر ﻛﺎﻣﻞ
ﺳﻠﻮﻟﻲ ﻗﺮار دارد ﺑﻴﺸﺘﺮ اﻳﻦ ﺗﻐﻴﻴﺮات ﻛﻪ ﻋﻤﺪﺗﺎ ﺳﺮﻳﻊ و ﻃﻲ 24ﺳﺎﻋﺖ
ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار ﻧﮕﺮﻓﺘﻪ اﺳﺖ .در ﻣﻄﺎﻟﻌﻪ ،Tuncerﻏﻠﻈﺖ ﻣﻨﻴﺰﻳﻢ
)ﻓﻮاﺻﻞ ﻧﻤﻮﻧﻪﮔﻴﺮي در اﻳﻦ ﻣﻄﺎﻟﻌﻪ( ﻣﻲﺑﺎﺷﺪ در اﺛﺮ ﺟﺎﺑﻪﺟﺎﻳﻲ ﺑﻴﻦ
ﺗﻮﺗﺎل ﭘﺎﻳﻴﻦﺗﺮي در ﺧﻮن ﺑﻨﺪ ﻧﺎف و ﺧﻮن ﻣﺎدر در ﻧﻮزاداﻧﻲ ﺑﺎ
داﺧﻞ و ﺧﺎرج ﺳﻠﻮل ﻣﻲﺑﺎﺷﺪ .ﺑﻨﺎﺑﺮاﻳﻦ ﺑﺎ اﻓﺰاﻳﺶ ﺑﻴﻠﻲروﺑﻴﻦ ﻳﺎ در اﺛﺮ
ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﻧﻮزادان ﺳﺎﻟﻢ ﮔﺰارش ﻛﺮد و ﻧﺘﻴﺠﻪ
ﺗﺨﺮﻳﺐ ﺳﻠﻮلﻫﺎ ﻳﺎ ﺑﻪﻋﻨﻮان ﻣﻜﺎﻧﻴﺴﻢ دﻓﺎﻋﻲ ،اﻓﺰاﻳﺶ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ
ﮔﺮﻓﺖ ﻛﻪ ﻫﻴﭙﻮﻣﻨﻴﺰﻳﻤﻲ ﻧﺎﺷﻲ از ﺷﻴﻔﺖ داﺧﻞ ﺳﻠﻮﻟﻲ ﻳﻮن ﻣﻨﻴﺰﻳﻢ
ﭘﻼﺳﻤﺎ دارﻳﻢ .ﭼﻮن در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ارﺗﺒﺎﻃﻲ ﺑﻴﻦ ﺷﺪت ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ
ﻣﻲﺑﺎﺷﺪ .در ﻣﻄﺎﻟﻌﻪ ﺑﻌﺪي Tuncerﺳﻄﻮح ﻣﻨﻴﺰﻳﻢ ،روي و ﻣﺲ ﻳﻮﻧﻴﺰه
و ﻫﻴﭙﺮﻣﻨﻴﺰﻣﻲ ﻳﺎﻓﺖ ﻧﺸﺪ و ﺣﺘﻲ ﺑﺎ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻣﺘﻮﺳﻂ ﻧﻴﺰ
در ﺧﻮن ﺑﻨﺪ ﻧﺎف و ﺧﻮن ﻣﺤﻴﻄﻲ ﻧﻮزاداﻧﻲ ﺑﺎ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﻣﺘﻮﺳﻂ
اﻓﺰاﻳﺶ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﭘﻼﺳﻤﺎ ﻣﺸﺎﻫﺪه ﺷﺪ و ﺑﺮ ﻃﺒﻖ ﻧﺘﺎﻳﺞ ﺟﺪﻳﺪ
و ﻧﻮزاداﻧﻲ ﺑﺎ ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺷﺪﻳﺪ ﻛﻪ ﻧﻴﺎزﻣﻨﺪ ﺗﻌﻮﻳﺾ ﺧﻮن ﺷﺪﻧﺪ
ﺗﺤﻘﻴﻘﺎت روي ﻧﻘﺶ رﺳﭙﺘﻮر NMDAو ﻧﻘﺶ اﺛﺮ ﺗﺤﺮﻳﻜﻲ آن در ﺑﺮوز
در ﻣﻘﺎﻳﺴﻪ ﺑﺎ ﻧﻮزاداﻧﻲ ﺑﺪون ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ اﻧﺪازهﮔﻴﺮي ﺷﺪ و ﻧﺸﺎن
ﻧﻮروﺗﻮﻛﺴﻴﺴﻴﺘﻪ در ﻣﻮارد ﻫﻴﭙﻮﻛﺴﻲ و ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ و ﻧﻘﺶ ﻣﻨﻴﺰﻳﻢ
ﺑﻠﻮكﻛﻨﻨﺪه و ﺗﻨﻈﻴﻢﻛﻨﻨﺪه ﻳﻮن ﻣﻨﻴﺰﻳﻢ ﺑﺮ رﺳﭙﺘﻮر
NMDA
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
ﺑﻪ زردي ﻗﺒﻞ و ﺑﻌﺪ از ﻓﺘﻮﺗﺮاﭘﻲKhosravi ﻧﻮزادان ﻣﺒﺘﻼN.درetﺗﻮﺗﺎل al. ﻣﻘﺎﻳﺴﻪ ﺳﻄﺢ ﺳﺮﻣﻲ ﻣﻨﻴﺰﻳﻢ
436
ﺑﻨﺎﺑﺮاﻳﻦ ﻓﺘﻮﺗﺮاﭘﻲ ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺠﺮ.ﻧﻮروﺗﻮﻛﺴﻴﻚ ﺑﻴﻠﻲروﺑﻴﻦ اﺳﺘﻔﺎده ﻛﺮد
- از اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻧﺘﻴﺠﻪ ﮔﺮﻓﺘﻴﻢ ﻛﻪ در ﻫﻴﭙﺮﺑﻴﻠﻲ،در ﻣﻬﺎر اﻳﻦ رﺳﭙﺘﻮر
ﺑﻪ ﻛﺎﻫﺶ ﻣﻨﻴﺰﻳﻢ ﺗﻮﺗﺎل ﺳﺮﻣﻲ ﺷﻮد ﻛﻪ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺷﻮاﻫﺪ اﺳﺘﻔﺎده از
ﺑﺪن ﺑﻪﻋﻨﻮان ﻣﻜﺎﻧﻴﺴﻢ دﻓﺎﻋﻲ ﺑﺎ اﻓﺰاﻳﺶ ﺳﻄﺢ ﻣﻨﻴﺰﻳﻢ ﺧﺎرج،روﺑﻴﻨﻤﻲ
ﻣﻨﻴﺰﻳﻢ در درﻣﺎن ﺑﻴﻤﺎران ﺑﺎ زردي ﺑﺎﻻ ﺑﺎﻋﺚ ﻛﺎﻫﺶ ﺧﻄﺮ آﺳﻴﺐ ﻋﺼﺒﻲ
ﺳﻠﻮﻟﻲ ﺳﻌﻲ در ﻛﺎﻫﺶ اﺛﺮات ﻧﻮروﺗﻮﻛﺴﻴﻚ ﺑﻴﻠﻲروﺑﻴﻦ ﺑﺎ ﻣﻬﺎر رﺳﭙﺘﻮر
.ﻧﺎﺷﻲ از ﺑﻴﻠﻲروﺑﻴﻦ ﺧﻮاﻫﺪ ﺷﺪ
دارد و ﺷﺎﻳﺪ در ﺻﻮرت ﺗﺎﻳﻴﺪ ﻧﺘﺎﻳﺞ اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺑﺎ ﺳﺎﻳﺮ
NMDA
ﺑﺪﻳﻦوﺳﻴﻠﻪ از ﺳﺮﻛﺎر ﺧﺎﻧﻢ دﻛﺘﺮ ﻧﺴﺮﻳﻦ ﺧﺎﻟﺼﻲ ﻓﻮق:ﺳﭙﺎﺳﮕﺰاري
،ﻣﻄﺎﻟﻌﺎت ﺑﺘﻮان در ﻣﻮارد ﻫﻴﭙﺮﺑﻴﻠﻲروﺑﻴﻨﻤﻲ ﺷﺪﻳﺪ و ﺧﻄﺮ ﻛﺮﻧﻴﻜﺘﺮوس
ﺗﺨﺼﺺ ﻧﻮزادان ﻛﻪ اﻧﺠﺎم اﻳﻦ ﭘﮋوﻫﺶ ﺑﺪون ﻫﻤﻜﺎري اﻳﺸﺎن ﻣﻴﺴﺮ
ﻫﻤﺮاه ﺳﺎﻳﺮ درﻣﺎنﻫﺎي ﻛﺎﻫﺶ ﺳﻄﺢ،از ﻣﻨﻴﺰﻳﻢ ﺑﻪﻋﻨﻮان درﻣﺎن ﻛﻤﻜﻲ
. ﺻﻤﻴﻤﺎﻧﻪ ﺗﺸﻜﺮ ﻣﻲﻧﻤﺎﻳﻢ،ﻧﺒﻮد
ﺑﻴﻠﻲروﺑﻴﻦ از ﺟﻤﻠﻪ ﻓﺘﻮﺗﺮاﭘﻲ و ﻳﺎ ﺗﻌﻮﻳﺾ ﺧﻮن ﺑﺮاي ﻛﺎﻫﺶ اﺛﺮات
1. Volpe JJ. Bilirubin and brain injury. In: Volpe JJ, editor. Neurology of Newborn. Philadelphia, PA: WB Saunders; 1995. p. 490-514. 2. Cashore WJ. Bilirubin metabolism and toxicity in the newborn. In: Polin RA, Fox WW, editors. Fetaland Neonatal Physiology. Philadelphia, PA: WB Saunders; 1998. p. 1493-8. 3. Hoffman DJ, Zanelli SA, Kubin J, Mishra OP, DelivoriaPapadopoulos M. The in vivo effect of bilirubin on the N-methyl-Daspartate receptor/ion channel complex in the brains of newborn piglets. Pediatr Res 1996;40(6):804-8. 4. Johnston M, McDonald M, Chen C, Trescher W. Role of excitatory amino acid receptors in perinatal hypoxic-ischemic brain injury. In: Meldrum BS, Moroni F, Simon RP, Woods JH, editors. Excitatory Amino Acids. New York: Raven Press; 1991. p. 711-6.
5. Sarici SU, Serdar MA, Erdem G, Alpay F. Evaluation of plasma ionized magnesium levels in neonatal hyperbilirubinemia. Pediatr Res 2004;55(2):243-7. 6. Tunçer M, Yenice A, Ozand P. Serum Mg, Ca, total protein levels in maternal and cord blood and its clinical significance. Turk J Pediatr 1972;14(1):13-22. 7. Misra PK, Kapoor RK, Dixit S, Seth TD. Trace metals in neonatal hyperbilirubinemia. Indian Pediatr 1988;25(8):761-4. 8. Pintov S, Kohelet D, Arbel E, Goldberg M. Predictive inability of cord zinc, magnesium and copper levels on the development of benign hyperbilirubinemia in the newborn. Acta Paediatr 1992;81(11):868-9. 9. Sarici SU, Kul M, Alpay F. Neonatal jaundice coinciding with or resulting from urinary tract infections? Pediatrics 2003;112(5):1212-3; author reply 1212-3.
References
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
Tehran University Medical Journal;ﻫﻤﻜﺎران Vol. 69, وNo. 7, October 2011: 432-437
100
Total serum magnesium level in icteric neonates before and after phototherapy
Abstract Nastaran Khosravi M.D. Alireza Aminian M.D.* Reza Taghipour M.D. Department of Neonatology, Aliasgar Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Received: May 04, 2011 Accepted: July 04, 2011
Background: Deposition of bilirubin in neurons causes permanent neuronal injury. Bilirubin exhibits an affinity for the phospholipids of plasma membrane like N-methylD-aspartate (NMDA) receptors. Magnesium is an NMDA antagonist and it acts against the neurotoxic effects of bilirubin. We compared pre- and post-phototherapy serum magnesium level of neonates with hyperbilirubinemia to find the best time of discharge and evaluate new management techniques such as magnesium supplementation. Methods: In this semi-experimental study, we evaluated neonates admitted in Ali Asghar Children’s Hospital in Tehran, Iran with signs of icter from 2009 to 2010. The inclusion criteria included age less than four weeks, no history of magnesium sulfate administration in the mother and absence of sepsis. Results: From 106 patients with icter, 50.9% were male and 49.1% were female neonates. Their mean gestational age was 37.341.286 (33-41) weeks and the mean birth weight was 3172.12436.936 (2022-4300) grams. The frequency of underlying causes of hyperbillirubinemia included: ABO mismatch 9.34%, Rh incompatibility 4.7%, breastfeeding 16% and breast milk 44.3%. There was a significant difference (P≤0.001) between serum magnesium levels before (2.24mg/dl) and after phototherapy (2.12mg/dl). There were no significant differences between serum magnesium values in the two sexes (male=2.28, female=2.19), among different gestational age groups (<34 wks=2.35, 35-37 wks=2.27, >38 wks=2.17), between different birth weight groups (15002500 g=2.4 and >2500 g=2.23) or severity of hyperbilirubinemia (mild=2.23,
moderate=2.21 and severe=2.29). Conclusion: Phototherapy decreases the total magnesium concentration and magnesium administration will prevent bilirubin neurotoxicity in icteric neonates. *
Corresponding author: Aliasghar Hospital, Khanevade’s Army Hospital, Kaj St., Shariati Ave., Tehran, Iran. Tel: +98-21-77603100 E-mail: dr.aminian@gmail.com
Keywords: Hyperbillirubinemia, magnesium, phototherapy.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
ﺑﻴﻤﺎر ﻣﻬﺮ 438-444 ،1390 ﺷﻤﺎره ،7 دوره ، 69 ﻣﺰاﻧﺸﻴﻤﺎلﻜﻲ داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷ ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ، ﺑﺮرﺳﻲ 24 ﺗﻬﺮان،ﻣﻌﺪه: ﻣﺮي و ﺗﻮﻣﻮرﻫﺎي
ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه :ﺑﺮرﺳﻲ 24ﺑﻴﻤﺎر
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1389/11/11 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/04/06 :
ﭼﻜﻴﺪه
*1
رﺿﺎ ﺑﺎﻗﺮي
زﻣﻴﻨﻪ و ﻫﺪف :ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﮔﻮارﺷﻲ ﺟﺰو ﺗﻮﻣﻮرﻫﺎي ﺑﺎ ﻣﻨﺸﺎء ﻋﻀﻼت ﺻﺎف ﻃﺒﻘﻪﺑﻨﺪي ﻣﻲﺷﺪﻧﺪ.
2
ﻗﺪرت اﷲ ﻣﺪاح
) Gastrointestinal Stromal Tumors (GISTﺷﺎﻳﻊﺗﺮﻳﻦ ﻧﻮع ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﮔﻮارﺷﻲ ﻫﺴﺘﻨﺪ ﻛﻪ در ﺳﺮﺗﺎﺳﺮ ﻟﻮﻟﻪ
2
ﻋﻠﻴﺮﺿﺎ ﺗﻮﺳﻠﻲ
ﮔﻮارش از ﻣﺮي ﺗﺎ آﻧﻮس دﻳﺪه ﻣﻲﺷﻮد و اﻛﺜﺮ ﻣﻮارد آن در ﻣﻌﺪه اﺗﻔﺎق ﻣﻲاﻓﺘﺪ .ﺑﻴﺸﺘﺮ ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ
3
ﻓﺎﻃﻤﻪ ﻧﻘﻮي رﻳﺎﺑﻲ
ﻋﻼﻣﺖ ﻫﺴﺘﻨﺪ و درﻣﺎن آن در اﻛﺜﺮ ﻣﻮارد ﺟﺮاﺣﻲ اﺳﺖ .ﻫﺪف ﻣﺎ در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺑﺮرﺳﻲ
GIST
GIST
ﺑﺪون
ﺗﻮﻣﻮرﻫﺎي ﻣﺮي و
-1ﮔﺮوه ﺟﺮاﺣﻲ ﺗﻮراﻛﺲ ،ﺑﻴﻤﺎرﺳﺘﺎن ﻗﺎﺋﻢ
ﻣﻌﺪه ﺑﻮده اﺳﺖ .روش ﺑﺮرﺳﻲ :در ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﮔﺬﺷﺘﻪﻧﮕﺮ ﺑﻴﻤﺎراﻧﻲ ﻛﻪ ﺑﻴﻦ ﺳﺎلﻫﺎي 1370ﺗﺎ 1388ﺑﺎ ﺗﺸﺨﻴﺺ
-2ﮔﺮوه ﺟﺮاﺣﻲ ﻋﻤﻮﻣﻲ ،ﺑﻴﻤﺎرﺳﺘﺎن ﻗﺎﺋﻢ
ﺗﻮﻣﻮر ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه در ﺑﻴﻤﺎرﺳﺘﺎن ﻗﺎﺋﻢ )ﻋﺞ( و اﻣﻴﺪ ﻣﺸﻬﺪ ﺑﺴﺘﺮي و ﺗﺤﺖ درﻣﺎن ﻗﺮار ﮔﺮﻓﺘﻪ ﺑﻮدﻧﺪ ﻣﻮرد
-3ﮔﺮوه ﺟﺮاﺣﻲ ﻋﻤﻮﻣﻲ
ﺑﺮرﺳﻲ ﻗﺮار ﮔﺮﻓﺘﻨﺪ .ﻳﺎﻓﺘﻪﻫﺎ 24 :ﺑﻴﻤﺎر وارد ﻣﻄﺎﻟﻌﻪ ﺷﺪﻧﺪ ) 16ﻧﻔﺮ ﻣﺮد و ﻫﺸﺖ ﻧﻔﺮ زن( ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ 50ﺳﺎل
داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﻣﺸﻬﺪ،
ﺑﻮد ،ﺷﺎﻳﻊﺗﺮﻳﻦ ﻣﺤﻞ ﺗﻮﻣﻮر در ﻓﻮﻧﺪوس ﻣﻌﺪه ﺑﻮد .ﺗﻤﺎم ﺑﻴﻤﺎران در ﺣﻴﻦ ﺗﺸﺨﻴﺺ ﻋﻼﻣﺖدار ﺑﻮده و ﺷﺎﻳﻊﺗﺮﻳﻦ
ﻣﺸﻬﺪ ،اﻳﺮان.
ﻋﻼﻣﺖ در ﺑﻴﻤﺎران اﺣﺴﺎس ﭘﺮي ﺑﻮد ﻛﻪ در %50از ﺑﻴﻤﺎران وﺟﻮد داﺷﺖ .ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻤﻞ ﺟﺮاﺣﻲ اﻧﺠﺎمﺷﺪه در اﻳﻦ ﺑﻴﻤﺎران ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ ﺳﺎبﺗﻮﺗﺎل ﺑﻮد .ﻣﺮگ و ﻣﻴﺮ ﺑﻴﻤﺎرﺳﺘﺎﻧﻲ ﺛﺒﺖ ﻧﺸﺪه ﺑﻮد .ﻋﻮارض در ﭘﻨﺞ ﺑﻴﻤﺎر )(%20/5 ﺑﻌﺪ از ﻋﻤﻞ دﻳﺪه ﺷﺪ ﻛﻪ ﺷﺎﻳﻊﺗﺮﻳﻦ آن اﻳﻠﺌﻮس ﺑﻌﺪ از ﻋﻤﻞ ﺑﻮده اﺳﺖ ،درﻣﺎن ﻛﻤﻜﻲ ﺑﻌﺪ از ﻋﻤﻞ ﻛﻪ در ﻫﺸﺖ ﺑﻴﻤﺎر ) (%33/1اﺳﺘﻔﺎده ﮔﺮدﻳﺪ ،در ﭘﻲﮔﻴﺮي ﺳﻪ ﺳﺎﻟﻪ ﺗﻨﻬﺎ ﺳﻪ ﺑﻴﻤﺎر ﻓﻮت ﻧﻤﻮدﻧﺪ ) .(%12/45ﻧﺘﻴﺠﻪﮔﻴﺮي :ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ
*
ﻧﺘﺎﻳﺞ ﻣﻨﺎﺳﺐ ﺟﺮاﺣﻲ در اﻳﻦ ﺑﻴﻤﺎران ﺑﺎ ﻋﻮارض ﻣﺮگ و ﻣﻴﺮ اﻧﺪك ،ﺟﺮاﺣﻲ ﺑﻪﻋﻨﻮان درﻣﺎن اﻧﺘﺨﺎﺑﻲ در ﺑﻴﻤﺎراﻧﻲ ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﻣﺸﻬﺪ ،ﺑﻴﻤﺎرﺳﺘﺎن ﻗﺎﺋﻢ )ﻋﺞ( ،ﻣﺮﻛﺰ
ﺗﺤﻘﻴﻘﺎت ﺟﺮاﺣﻲ آﻧﺪوﺳﻜﻮﭘﻴﻚ و روشﻫﺎي ﻛﻢﺗﻬﺎﺟﻤﻲ داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﻣﺸﻬﺪ
ﻛﻪ ﺗﻮاﻧﺎﻳﻲ ﺟﺮاﺣﻲ را دارﻧﺪ ﺗﻮﺻﻴﻪ ﻣﻲﮔﺮدد.
ﺗﻠﻔﻦ0511-8012806 :
E-mail: Bagherir@mums.ac.ir
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :ﺗﻮﻣﻮر ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه ،ﺗﺸﺨﻴﺺ ،درﻣﺎن ،ﻋﻮارض ،ﻣﺮگ و ﻣﻴﺮ.
اﻳﻦ ﺗﻮﻣﻮرﻫﺎ ،واﺑﺴﺘﮕﻲ ﻧﺰدﻳﻜﻲ ﺑﺎ ﻳﻜﻲ از ﺳﻠﻮلﻫﺎي ﺑﺎﻓﺖ ﺑﻴﻨﺎﺑﻴﻨﻲ
ﻣﻘﺪﻣﻪ
ﺑﻪﻧﺎم Cajalدارﻧﺪ .اﻳﻦ ﺳﻠﻮلﻫﺎ ﺣﺎوي
ﺗﺎ ﺣﺪود 20ﺳﺎل ﻗﺒﻞ اﻛﺜﺮ ﻣﻮارد ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﮔﻮارﺷﻲ
C-Kit
و
و از ﻧﻈﺮ اﻳﻤﻮﻧﻮﻫﻴﺴﺘﻮﺷﻴﻤﻲ از ﻧﻈﺮ دﺳﻤﻴﻦ و GIST
CD117 S100
و
CD34
ﻫﺴﺘﻨﺪ 5و4
ﻣﻨﻔﻲ ﻫﺴﺘﻨﺪ.
ﺟﺰء ﺗﻮﻣﻮرﻫﺎي ﺑﺎ ﻣﻨﺸﺎ ﻋﻀﻼت ﺻﺎف ﻃﺒﻘﻪﺑﻨﺪي ﻣﻲﺷﺪﻧﺪ .در ﺳﺎل
ﺷﻴﻮع
Mazur ،1984و Clarkﮔﺰارش ﻛﺮدﻧﺪ ﻛﻪ ﺗﻌﺪاد زﻳﺎدي از ﺗﻮﻣﻮرﻫﺎﻳﻲ
و ﭘﻨﺞ درﺻﺪ از ﺗﻤﺎم ﻣﻮارد ﺳﺎرﻛﻮمﻫﺎي ﮔﺰارش ﺷﺪه را ﺷﺎﻣﻞ 7و6
زﻳﺎد ﻧﻴﺴﺖ و ﺣﺪود %0/1-3ﻛﻞ ﻧﺌﻮﭘﻼﺳﻢﻫﺎي ﮔﻮارﺷﻲ
و اﻛﺜﺮ ﻣﻮارد آن در ﻣﺤﺪوده ﺳﻨﻲ 40-60ﺳﺎل اﺗﻔﺎق
ﻛﻪ ﺟﺰ ﺗﻮﻣﻮرﻫﺎي ﻋﻀﻼت ﺻﺎف ﻣﺤﺴﻮب ﻣﻲﺷﻮﻧﺪ ،داراي ﺷﻮاﻫﺪ
ﻣﻲﺷﻮد
اﻳﻤﻮﻧﻮﻫﻴﺴﺘﻮﺷﻴﻤﻴﺎﻳﻲ و ﻣﻴﻜﺮوﺳﻜﻮپ اﻟﻜﺘﺮوﻧﻲ ﻋﻀﻼت ﺻﺎف و
ﻣﻲاﻓﺘﺪ ،اﻣﺎ ﺗﻔﺎوت ﺟﻨﺴﻲ واﺿﺤﻲ در آن ﻣﺸﺎﻫﺪه ﻧﻤﻲﺷﻮد .اﻟﺒﺘﻪ در
ﻏﻼف ﻋﺼﺒﻲ ﻧﻴﺴﺘﻨﺪ و اﺻﻄﻼح ﺗﻮﻣﻮرﻫﺎي اﺳﺘﺮوﻣﺎﻳﻲ ﻣﻌﺪه
ﺑﻌﻀﻲ ﻣﻄﺎﻟﻌﺎت ﺑﻴﺸﺘﺮﻳﻦ ﺷﻴﻮع ﺳﻨﻲ را در ﺑﺎزده زﻣﺎﻧﻲ 55-65ﺳﺎل
2و1
) Gastrointestinal Stromal Tumor (GISTرا ﭘﻴﺸﻨﻬﺎد ﻛﺮدﻧﺪ.
1
4
GIST
ذﻛﺮ ﻛﺮدهاﻧﺪ .ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ اﻛﺜﺮ ﻣﻮارد آن در ﻣﻌﺪه )(%40-70
ﺷﺎﻳﻊﺗﺮﻳﻦ ﻧﻮع ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﮔﻮارﺷﻲ ﻫﺴﺘﻨﺪ ﻛﻪ از ﻣﺮي ﺗﺎ
اﺗﻔﺎق ﻣﻲاﻓﺘﺪ اﻣﺎ ﺑﺮوز آن در روده ﺑﺎرﻳﻚ و ﻣﺰاﻧﺘﺮ ﻧﻴﺰ ﺷﺎﻳﻊ اﺳﺖ
آﻧﻮس دﻳﺪه ﻣﻲﺷﻮﻧﺪ 3.در ﺣﺎل ﺣﺎﺿﺮ روﺷﻦ ﺷﺪه اﺳﺖ ﻛﻪ ﺳﻠﻮلﻫﺎي
) %5 .(%20-40ﻣﻮارد آن در ﻣﺮي و %5-15آن در ﻛﻮﻟﻮن و رﻛﺘﻮم
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
رﺿﺎ ﺑﺎﻗﺮي و ﻫﻤﻜﺎران
9و8
ﮔﺰارش ﺷﺪه اﺳﺖ.
ﺑﻴﺶﺗﺮ ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ
GIST
ﺑﺪون ﻋﻼﻣﺖ
439
ﻳﺎﻓﺘﻪﻫﺎ
ﻫﺴﺘﻨﺪ اﻣﺎ در ﻣﻮارد ﭘﻴﺶرﻓﺘﻪ ﻋﻼﻳﻢ ﺗﻮده ﺷﻜﻤﻲ ،درد ﺷﻜﻢ ﻳﺎ 10و3
ﺣﺪاﻗﻞ %10-30ﻣﻮارد ﺑﻪﺻﻮرت اﺗﻔﺎﻗﻲ
ﺑﻪﻃﻮر ﻛﻠﻲ 24ﺑﻴﻤﺎر در ﻓﺎﺻﻠﻪ زﻣﺎﻧﻲ 1370-88در اﻳﻦ ﺑﻴﻤﺎرﺳﺘﺎن
در ﺣﻴﻦ ﻻﭘﺎراﺗﻮﻣﻲ ﻳﺎ آﻧﺪوﺳﻜﻮﭘﻲ ﻳﺎ ﺑﺮرﺳﻲﻫﺎي ﺗﺼﻮﻳﺮﺑﺮداري ﻛﺸﻒ
ﺑﺎ ﺗﺸﺨﻴﺺ ﺗﻮﻣﻮر ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه ﺑﺴﺘﺮي ﺷﺪه ﺑﻮدﻧﺪ ﻛﻪ از
ﺧﻮد را ﺑﺎ ﻣﺘﺎﺳﺘﺎز ﻧﺸﺎن
ﺑﻴﻦ اﻳﻦ ﺑﻴﻤﺎران 16ﻧﻔﺮ ﻣﺮد ) (%66و ﻫﺸﺖ ﻧﻔﺮ زن ) (%34ﺑﻮدﻧﺪ.
ﺣﺬف ﺟﺮاﺣﻲ اﺳﺖ .ﺑﺎﻳﺪ ﺗﻼش
ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ ﺑﻴﻤﺎران 50ﺳﺎل ﺑﻮد )ﺟﻮانﺗﺮﻳﻦ ﺑﻴﻤﺎر 14ﺳﺎﻟﻪ و
ﺷﻮد ﻛﻪ در ﺣﺪ اﻣﻜﺎن ﺗﻤﺎم ﺗﻮﻣﻮر ﺑﻪﺻﻮرت ﻛﺎﻣﻞ ﺧﺎرج ﺷﻮد و ﻫﻤﺮاه
ﻣﺴﻦﺗﺮﻳﻦ آنﻫﺎ 76ﺳﺎﻟﻪ ﺑﻮده اﺳﺖ( .ﺷﺎﻳﻊﺗﺮﻳﻦ ﻣﺤﻞ ﺗﻮﻣﻮر در
ﺑﺎ آن ﻗﺴﻤﺘﻲ از ﺑﺎﻓﺖ ﺳﺎﻟﻢ و ﻧﻴﺰ ارﮔﺎنﻫﺎي ﻣﺠﺎور در ﺻﻮرت
ﻓﻮﻧﺪوس ﻣﻌﺪه ﺑﻮد ﻛﻪ ﺷﺎﻣﻞ ﻫﺸﺖ ﺑﻴﻤﺎر ) (%34ﻣﻲﺷﺪ .ﺳﺎﻳﺮ ﻣﻨﺎﻃﻖ
GIST
درﮔﻴﺮ ﺑﻪﺗﺮﺗﻴﺐ ﺷﻴﻮع ﻋﺒﺎرت ﺑﻮدﻧﺪ از :ﺟﺴﻢ ﻣﻌﺪه )ﭘﻨﺞ ﺑﻴﻤﺎر(
ﺑﻪﻧﺪرت ﺑﻪ ﮔﺮهﻫﺎي ﻟﻨﻔﺎوي ﻣﺘﺎﺳﺘﺎز ﻣﻲدﻫﺪ و ﺑﻪﻫﻤﻴﻦ ﺟﻬﺖ
،%20/5ﺛﻠﺚ ﻣﻴﺎﻧﻲ ﻣﺮي )ﭼﻬﺎر ﺑﻴﻤﺎر( ،%16/6اﻧﺘﺮوم )دو ﺑﻴﻤﺎر( ،%8/3
ﻟﻨﻔﺎدﻧﻜﺘﻮﻣﻲ در ﻣﻮرد اﻳﻦ ﺗﻮﻣﻮرﻫﺎ ﻣﻌﻤﻮل ﻧﻴﺴﺖ 1.ﺑﺮداﺷﺖ ﮔﻮهاي در
ﺟﺴﻢ ﻣﻌﺪه و اﻧﺘﺮوم )دو ﺑﻴﻤﺎر( ،%8/3ﻳﻚﺳﻮم ﺗﺤﺘﺎﻧﻲ و ﻳﻚﺳﻮم
ﻣﻌﺪه ﻳﺎ ﺣﺬف ﻳﻚ ﻗﺴﻤﺖ از روده ﺑﺎرﻳﻚ ﺑﺮاي درﻣﺎن ﺟﺮاﺣﻲ ﻛﻔﺎﻳﺖ
ﻣﻴﺎﻧﻲ ﻣﺮي )دو ﺑﻴﻤﺎر( %8/3و ﻳﻚﺳﻮم ﭘﺮوﮔﺰﻳﻤﺎل ﻣﺮي )ﻳﻚ ﺑﻴﻤﺎر(
ﻣﻲﻛﻨﺪ و ﺟﺮاﺣﻲﻫﺎي ﺑﺰرگﺗﺮ ﻧﺘﺎﻳﺞ و ﭘﻴﺶآﮔﻬﻲ ﺑﻬﺘﺮي در ﺑﺮ ﻧﺨﻮاﻫﺪ
.%4/15ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻼﻳﻢ ﺑﻴﻤﺎران ﻫﻨﮕﺎم ﻣﺮاﺟﻌﻪ اﺣﺴﺎس ﭘﺮي ﺑﻮد ﻛﻪ
ﻛﺮد 1.رادﻳﻮﺗﺮاﭘﻲ در اﻳﻦ ﺑﻴﻤﺎران اﺛﺮ زﻳﺎدي ﻧﺪارد .ﻗﺒﻞ از اﻳﻦﻛﻪ
در %50از ﺑﻴﻤﺎران وﺟﻮد داﺷﺖ .ﺳﺎﻳﺮ ﻋﻼﻳﻢ ﺑﻪﺗﺮﺗﻴﺐ ﺷﻴﻮع در
ﺧﻮنرﻳﺰي دﻳﺪه ﻣﻲﺷﻮد.
ﻣﻲﺷﻮﻧﺪ و ﺣﺪود %15-50ﻣﻮارد ﻣﻲدﻫﻨﺪ 10.اﺻﻠﻲﺗﺮﻳﻦ درﻣﺎن
GIST
GIST
درﮔﻴﺮي ﺧﺎرج ﺷﻮﻧﺪ 8.ﺑﺮﺧﻼف آدﻧﻮﻛﺎرﺳﻴﻨﻮمﻫﺎي ﮔﻮارﺷﻲ،
ﻣﻬﺎرﻛﻨﻨﺪهﻫﺎي ﺗﻮﻣﻮرﻫﺎي
KIT
GIST
ﺑﻪﻧﺎم Imatinibﺗﻮﻟﻴﺪ ﺷﻮﻧﺪ ﺑﻪﻧﻈﺮ ﻣﻲرﺳﻴﺪ ﻛﻪ 12و11
ﺑﻪ ﺷﻴﻤﻲدرﻣﺎﻧﻲ ﭘﺎﺳﺦ ﻗﺎﺑﻞ ﻗﺒﻮﻟﻲ ﻧﻤﻲدادﻧﺪ،
ﺟﺪول 1آورده ﺷﺪه اﺳﺖ .ﺑﺮاي ﺗﺸﺨﻴﺺ ﻗﺒﻞ از ﻋﻤﻞ در ﺑﻴﻤﺎران روشﻫﺎي ﻣﺨﺘﻠﻔﻲ از ﺟﻤﻠﻪ آﻧﺪوﺳﻜﻮﭘﻲ ،ﺑﻠﻊ ﺑﺎرﻳﻢ و
CT Scan
و
وﻟﻲ اﻣﺮوزه Imatinibدرﻣﺎن اﻧﺘﺨﺎﺑﻲ اﻧﻮاع ﻏﻴﺮﻗﺎﺑﻞ ﺑﺮداﺷﺖ ﻳﺎ
ﺳﻮﻧﻮﮔﺮاﻓﻲ اﻧﺠﺎم ﺷﺪه ﺑﻮد .در 18ﻣﻮرد از ﺑﻴﻤﺎران ) (%75آﻧﺪوﺳﻜﻮﭘﻲ
ﻣﺘﺎﺳﺘﺎﺗﻴﻚ GISTﺷﺪه اﺳﺖ 4.ﺣﺬف ﻛﺎﻣﻞ ﺟﺮاﺣﻲ در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ
ﺑﻪﺗﺸﺨﻴﺺ ﻛﻤﻚ ﻛﺮده ﺑﻮد و در ﻫﺸﺖ ﻣﻮرد ) (%33ﻧﻴﺰ ﺑﻠﻊ ﺑﺎرﻳﻮم
ﺑﻘﺎي ﭘﻨﺞ ﺳﺎﻟﻪ %48-65اﻳﺠﺎد ﺧﻮاﻫﺪ ﻛﺮد 1.ﻣﺎ در اﻳﻦ ﻣﻄﺎﻟﻌﻪ
ﻧﺸﺎندﻫﻨﺪه ﺿﺎﻳﻌﻪ ﺑﻮد CT Scan .در ﺗﻤﺎﻣﻲ ﺑﻴﻤﺎران ﻗﺒﻞ از ﻋﻤﻞ اﻧﺠﺎم
ﻣﺮي ﻣﻌﺪه در ﺑﻴﻤﺎران ﻣﺮاﺟﻌﻪﻛﻨﻨﺪه
ﺷﺪ .ﺷﻜﻞ 1ﻧﻤﺎي ﺑﻠﻊ ﺑﺎرﻳﻢ ﺑﻴﻤﺎر ﺑﺎ ﻟﻴﻮﻣﻴﻮﻣﺎي ﻣﺮي را ﻧﺸﺎن ﻣﻲدﻫﺪ
GIST
ﺑﻪ ﺑﺮرﺳﻲ ﻣﻮارد ﺗﻮﻣﻮرﻫﺎي
GIST
ﺑﻪ دو ﻣﺮﻛﺰ ﻗﺎﺋﻢ و اﻣﻴﺪ ﻣﺸﻬﺪ ﻃﻲ ﺳﺎلﻫﺎي 1370-88ﭘﺮداﺧﺘﻴﻢ.
و ﺷﻜﻞ 2ﺳﻲﺗﻲاﺳﻜﻦ ﺑﻴﻤﺎر ﻣﺒﺘﻼ ﺑﻪ GISTﻣﻌﺪه را ﻧﺸﺎن ﻣﻲدﻫﺪ .از ﺑﻴﻦ اﻳﻦ 24ﺑﻴﻤﺎر در زﻣﺎن ﻣﺮاﺟﻌﻪ ﺳﻪ ﻣﻮرد ﺿﺎﻳﻌﻪ وﺳﻴﻊ ﺑﺎ درﮔﻴﺮي
روش ﺑﺮرﺳﻲ
اﺣﺸﺎي ﻣﺠـﺎور )ﻃﺤﺎل( و دو ﻣـﻮرد ﻣﺘﺎﺳﺘﺎز ﻛﺒـﺪي ﻫﻢزﻣـﺎن ﻣﺸﺎﻫﺪه
در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﮔﺬﺷﺘﻪﻧﮕﺮ و Case-seriesﺑﻴﻤﺎران ﺑﺴﺘﺮي ﺷﺪه در ﺑﻴﻤﺎرﺳﺘﺎنﻫﺎي ﻗﺎﺋﻢ و اﻣﻴﺪ ﻣﺸﻬﺪ ﻃﻲ ﺳﺎلﻫﺎي 1370-88ﻛﻪ ﺑﺎ ﺗﺸﺨﻴﺺ ﻧﻬﺎﻳﻲ ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه ﺑﻮد ﺗﺤﺖ درﻣﺎن
ﺟﺪول :1-ﻋﻼﻳﻢ ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه ﻫﻨﮕﺎم ﻣﺮاﺟﻌﻪ )در ﺑﻌﻀﻲ از ﺑﻴﻤﺎران ﺑﻴﺶ از ﻳﻚ ﻋﻼﻣﺖ وﺟﻮد داﺷﺘﻪ اﺳﺖ(
ﻗﺮار ﮔﺮﻓﺘﻪ ﺑﻮدﻧﺪ ،ﺑﺮرﺳﻲ ﺷﺪﻧﺪ .در اﻳﻦ ﺑﻴﻤﺎران درﻣﺎن ﺟﺮاﺣﻲ و
ﻋﻼﻳﻢ
ﻓﺮاواﻧﻲ
درﺻﺪ
ﻛﻤﻮرادﻳﻮﺗﺮاﭘﻲ ﺑﺮاﺳﺎس ﺷﺮاﻳﻂ ﺑﻴﻤﺎر اﻧﺠﺎم ﺷﺪه اﺳﺖ .اﻃﻼﻋﺎت
اﺣﺴﺎس ﭘﺮي
12
%50
ﺑﻴﻤﺎران ﺷﺎﻣﻞ ﺳﻦ و ﺟﻨﺲ و ﻋﻼﻳﻢ ﺑﺎﻟﻴﻨﻲ ﻫﻨﮕﺎم ﻣﺮاﺟﻌﻪ ،روش
ﺑﻲاﺷﺘﻬﺎﻳﻲ
10
%42
ﻛﺎﻫﺶ وزن
8
%33
دﻳﺴﻔﺎژي
7
%29
ﺗﻮده ﺷﻜﻤﻲ
5
%21
درﻣﺎن ﻗﺮار ﮔﺮﻓﺘﻪ و اﻃﻼﻋﺎت از ﭘﺮوﻧﺪهﻫﺎي ﻣﻮﺟﻮد ﮔﺮدآوري ﺷﺪﻧﺪ.
درد ﺷﻜﻢ
4
%17
ﭘﺲ از ﺟﻤﻊآوري اﻃﻼﻋﺎت و رﺳﻢ ﺟﺪاول ﻓﺮاواﻧﻲ و ﻧﻤﻮدارﻫﺎ ،آﻧﺎﻟﻴﺰ
ﺗﻬﻮع و اﺳﺘﻔﺮاغ
1
%4
ﺗﻮﺳﻂ ﻧﺮماﻓﺰار SPSSوﻳﺮاﺳﺖ 11/5اﻧﺠﺎم ﺷﺪ.
ﻫﻤﺎﺗﻤﺰ
1
%4
ﺗﺸﺨﻴﺼﻲ ،ﻧﻮع ﺑﺎﻓﺖﺷﻨﺎﺳﻲ ﺗﻮﻣﻮر ،ﻧﻮع درﻣﺎن اﻧﺠﺎمﺷﺪه و ﻋﻮارض ﻣﺮﺑﻮط ﺑﻪ درﻣﺎن ﻣﺮگ و ﻣﻴﺮ ﺑﻴﻤﺎرﺳﺘﺎﻧﻲ و ﻃﻮل ﻋﻤﺮ ﺳﻪ ﺳﺎل ﺑﻌﺪ از
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
440
ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه :ﺑﺮرﺳﻲ 24ﺑﻴﻤﺎر
ﺷﻜﻞ :3-ﻣﺘﺎﺳﺘﺎز ﻛﺒﺪي GISTﺗﻮﻣﻮر ﻣﻌﺪه
ﺷﻜﻞ :1-ﺑﻠﻊ ﺑﺎرﻳﻢ ﺿﺎﻳﻌﻪ ﻟﻴﻮﻣﻴﻮم ﻣﺮي
ﺟﺪول :2-اﻋﻤﺎل ﺟﺮاﺣﻲ در ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه ﻓﺮاواﻧﻲ
درﺻﺪ
ﻧﻮع ﻋﻤﻞ ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ ﺳﺎب ﺗﻮﺗﺎل
7
%29
ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ ﺗﻮﺗﺎل
6
%25
اﻧﻮﻛﻠﺌﺎﺳﻴﻮن ﺗﻮﻣﻮر از ﻣﺮي
4
%16
رزﻛﺴﻴﻮن ﮔﻮه اي ﻣﻌﺪه
5
%20
ازوﻓﺎژﻛﺘﻮﻣﻲ ﺗﺮاﻧﺲ ﺗﻮراﺳﻴﻚ
1
%5
ازوﻓﺎژﻛﺘﻮﻣﻲ ﺗﺮاﻧﺲ ﻫﻴﺎﺗﺎل
1
%5
ﻣﺠﻤﻮع
24
%100
ﻟﻴﻮﻣﻴﻮﺳﺎرﻛﻮم و ﻳﻚ ﺑﻴﻤﺎر ) (%4/1ﻟﻴﻮﻣﻴﻮﺑﻼﺳﺘﻮﻣﺎ ﮔﺰارش ﺷﺪه ﺑﻮد. ﺷﻜﻞ :2-در ﺳﻲﺗﻲاﺳﻜﻦ ﮔﺴﺘﺮش GISTﺗﻮﻣﻮر از ﺟﺪار ﻣﻌﺪه
ﻋﻮارض ﺑﻌﺪ از ﻋﻤﻞ ﻧﻴﺰ در ﭘﻨﺞ ﺑﻴﻤﺎر ) (%20/5ﺑﻴﻤﺎران ﻣﺸﺎﻫﺪه ﺷﺪه ﺑﻮد ﻛﻪ ﺑﻪﺗﺮﺗﻴﺐ ﺷﺎﻣﻞ اﻳﻠﺌﻮس ﺳﻪ ﺑﻴﻤﺎر ) (%13/3ﻋﻔﻮﻧﺖ زﺧﻢ ،ﻳﻚ ﺑﻴﻤﺎر ) (%4/1و آﺗﻠﻜﺘﺎزي ﻳﻚ ﺑﻴﻤﺎر ) (%4/1ﺑﻮدﻧﺪ ﻛﻪ ﻫﻤﻪ ﺑﻬﺒﻮد ﻛﺎﻣﻞ
ﺷﺪه ﺑﻮد .ﺷﻜﻞ 3ﻣﺘﺎﺳﺘﺎز ﻛﺒﺪي در ﺑﻴﻤﺎر ﻣﺒﺘﻼ ﺑﻪ GISTﻣﻌﺪه را ﻧﺸﺎن
ﭘﻴﺪا ﻛﺮدﻧﺪ ،ﻓﻴﺴﺘﻮل ﺑﻌﺪ از ﻋﻤﻞ دﻳﺪه ﻧﺸﺪ .در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﻫﺸﺖ ﺑﻴﻤﺎر
ﻣﻲدﻫﺪ .ﺟﻬﺖ اﻳﻦ ﺑﻴﻤﺎران روشﻫﺎي ﺟﺮاﺣﻲ ﻣﺨﺘﻠﻔﻲ ﺑﻪﻛﺎر رﻓﺘﻪ ﺑﻮد
ﺑﻌﺪ از ﺟﺮاﺣﻲ ﻧﻴﺎز ﺑﻪ درﻣﺎن ﻛﻤﻜﻲ داﺷﺘﻨﺪ ) ،(%33/1ﻛﻪ در ﭘﻨﺞ ﺑﻴﻤﺎر
ﻛﻪ ﺷﺎﻳﻊﺗﺮﻳﻦ آنﻫﺎ ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ ﺳﺎبﺗﻮﺗﺎل در %29از ﺑﻴﻤﺎران ﺑﻮد.
) (%20/5از Imatinibﺳﻮد ﺑﺮده ﻛﻪ از اﻳﻦ ﺑﻴﻤﺎران دو ﺑﻴﻤﺎر ﺑﺎ ﻣﺘﺎﺳﺘﺎز
روشﻫﺎي درﻣﺎﻧﻲ دﻳﮕﺮ ﺑﻪﺗﺮﺗﻴﺐ ﺷﻴﻮع در ﺟﺪول 2ﻧﺸﺎن داده
ﻛﺒﺪي در زﻣﺎن ﺗﺸﺨﻴﺺ ﺑﺎ دوز 600mgﺗﺤﺖ درﻣﺎن ﻗﺮار ﮔﺮﻓﺘﻪ و ﺗﺎ
ﺷﺪهاﻧﺪ .در ﺳﻪ ﻣﻮرد ) (%11/5از ﺑﻴﻤﺎران ﺿﻤﻦ اﻧﺠﺎم ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ
زﻣﺎن ﺣﻴﺎت ) 1/5و دو ﺳﺎل ﺑﻌﺪ از ﺟﺮاﺣﻲ اوﻟﻴﻪ( اﻳﻦ دارو را ﺑﺎ ﻛﻨﺘﺮل
ﺑﻪﻋﻠﺖ درﮔﻴﺮي ﻣﺠﺎورﺗﻲ اﺳﭙﻠﻨﻜﺘﻮﻣﻲ ﻧﻴﺰ اﻧﺠﺎم ﺷﺪه اﺳﺖ و در دو
آﻧﺰﻳﻢﻫﺎي ﻛﺒﺪي درﻳﺎﻓﺖ ﻛﺮدﻧﺪ و ﺳﻪ ﺑﻴﻤﺎر دﻳﮕﺮ ﺑﻪﻋﻨﻮان درﻣﺎن
ﺑﻴﻤﺎر ﻛﻪ ﻣﺘﺎﺳﺘﺎز ﻛﺒﺪي داﺷﺘﻨﺪ ﻧﻴﺰ ﺗﻮﻣﻮر ﺑﺎ ﺗﻮﺗﺎل ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ
ﻛﻤﻜﻲ در ﻓﺮمﻫﺎي ﮔﺴﺘﺮش ﻣﻮﺿﻌﻲ و ﺑﺪون ﻣﺘﺎﺳﺘﺎز دوردﺳﺖ ﺑﻪﻣﻴﺰان
ﺑﻪﺻﻮرت ﻛﺎﻣﻞ ﻗﺎﺑﻞ اﻧﺠﺎم ﺑﻮد و ﺗﻨﻬﺎ ﻧﻤﻮﻧﻪﺑﺮداري از ﻛﺒﺪ اﻧﺠﺎم
400mgﺗﺎ ﻳﻚﺳﺎل ﺑﻌﺪ از ﻋﻤﻞ دارو را درﻳﺎﻓﺖ ﻧﻤﻮدﻧﺪ .دو ﺑﻴﻤﺎر
ﺷﺪ .ﺷﻜﻞ 4ﻧﻤﺎي اﻧﻮﻛﻠﺌﺎﺳﻴﻮن را ﺣﻴﻦ ﺟﺮاﺣﻲ ﻟﻴﻮﻣﻴﻮﻣﺎي ﻣﺮي
ﺑﻪﻋﻠﺖ ﻟﻴﻮﻣﻴﻮﺳﺎرﻛﻮﻣﺎي ﻣﺮي ﺗﺤﺖ ﻛﻤﻮﺗﺮاﭘﻲ و رادﻳﻮﺗﺮاﭘﻲ ﺑﻌﺪ از
دﻳﺴﺘﺎل ﻧﺸﺎن ﻣﻲدﻫﺪ .ﻧﺘﻴﺠﻪ ﭘﺎﺗﻮﻟﻮژي در اﻳﻦ ﺑﻴﻤﺎران 12ﺑﻴﻤﺎر )(%50
ﻋﻤﻞ و ﻳﻚ ﺑﻴﻤﺎر ﻧﻴﺰ ﺑﻪﻋﻠﺖ ﻟﻴﻮﻣﻴﻮﺑﻼﺳﺘﻮﻣﺎي ﻣﺮي ﺗﺤﺖ ﻛﻤﻮﺗﺮاﭘﻲ
ﻣﻮارد ،GISTﻫﺸﺖ ﺑﻴـﻤﺎر ) (%33/1ﻣﻮارد ﻟﻴﻮﻣﻴﻮم ،ﺳﻪ ﺑﻴﻤﺎر )(%12/5
ﺑﻌـﺪ از ﻋﻤﻞ ﻗﺮار ﮔﺮﻓﺘﻨﺪ .در ﭘﻲﮔﻴـﺮي ﺳﻪ ﺳﺎل ﺑﻌـﺪ از درﻣـﺎن در دو
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
رﺿﺎ ﺑﺎﻗﺮي و ﻫﻤﻜﺎران
441
اﻳﻦ ﺑﻴﻤﺎران ﺛﺒﺖ ﺷﺪه اﺳﺖ 14.ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ ﺑﻴﻤﺎران ﺑﻴﻦ 53ﺗﺎ 49ﺳﺎل
اﻟﻒ
ﮔﺰارش ﮔﺮدﻳﺪه ﺑﻮد .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ ﺗﻔﺎوت زﻳﺎدي ﺑﻴﻦ ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ در ﻣﻄﺎﻟﻌﺎت وﺟﻮد ﻧﺪارد ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ ﭘﺮاﻛﻨﺪﮔﻲ ﺳﻨﻲ آن ﺗﺤﺖ ﺗﺄﺛﻴﺮ ﻋﻮاﻣﻞ ﻣﺤﻴﻄﻲ ﻧﻴﺴﺖ 15.در ﺑﺮﺧﻲ ﻣﻄﺎﻟﻌﺎت ذﻛﺮ ﺷﺪه ﻛﻪ ﺑﺮﺗﺮي واﺿﺢ ﺟﻨﺴﻲ در اﻳﻦ ﺑﻴﻤﺎران وﺟﻮد ﻧﺪارد 1.در ﻣﻄﺎﻟﻌﻪ Rabinﻛﻪ ﺑﻪ ﻣﺪت 19ﺳﺎل اﻳﻦ ﮔﺮوه ﺑﻴﻤﺎران را ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار داده ﺑﻮد ،ﻧﺴﺒﺖ ﺟﻨﺴﻲ ﻣﺮد ﺑﻪ زن 1/3ﺑﻪ ﻳﻚ ﺑﻪدﺳﺖ آﻣﺪه ﺑﻮد 16.در ﻣﻄﺎﻟﻌﻪ Hikiدر ﺳﺎل ،2008ﺗﻤﺎم ﺑﻴﻤﺎران ﻣﻮﻧﺚ ﺑﻮدﻧﺪ ﻛﻪ ﺑﺎ ﻫﻴﭻﻳﻚ از ﻣﻄﺎﻟﻌﺎت ﻗﺒﻠﻲ و اﻋﺪاد و ارﻗﺎم ﺛﺒﺖ ﺷﺪه در رﻓﺮﻧﺲﻫﺎي ﻗﺒﻠﻲ ﺗﺸﺎﺑﻪ و ﻫﻢﺧﻮاﻧﻲ ﻧﺪارد 15.در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﻣﺘﻮﺳﻂ ﺳﻨﻲ ﺑﻴﻤﺎران 50ﺳﺎل ﺑﻮده و ﺑﻴﻤﺎري در ﻣﺮدان ﺷﺎﻳﻊﺗﺮ ﺑﻮده اﺳﺖ .ﺑﺮرﺳﻲﻫﺎ ﻧﺸﺎن داده اﺳﺖ ﻛﻪ ﺑﺮوز
ب
ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﮔﻮارﺷﻲ ﺑﻪﺧﺼﻮص GISTدر ﺳﺮﺗﺎﺳﺮ ﻃﻮل ﻟﻮﻟﻪ ﮔﻮارش ﻳﻜﺴﺎن ﻧﻴﺴﺖ و در ﺑﻌﻀﻲ ﻗﺴﻤﺖﻫﺎ اﻳﻦ ﺗﻮﻣﻮرﻫﺎ ﺷﺎﻳﻊﺗﺮﻧﺪ. ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ ﺷﺎﻳﻊﺗﺮﻳﻦ ﻣﺤﻞ ﺑﺮاي اﻳﺠﺎد و ﺑﺮوز اﻳﻦ ﺗﻮﻣﻮرﻫﺎ 8و1
ﻣﻌﺪه ﺑﺎﺷﺪ
ﻛﻪ در ﻣﻮرد ﺑﻴﻤﺎران ﻣﺎ ﻧﻴﺰ اﻳﻦ ﻣﺴﺄﻟﻪ ﺻﺪق ﻣﻲﻛﺮد
ﺑﻪﻃﻮري ﻛﻪ در %71/5ﺑﻴﻤﺎران ﺗﻮﻣﻮر در ﻣﻌﺪه اﻳﺠﺎد ﺷﺪه ﺑﻮد و ﻓﻘﻂ ﺷﻜﻞ :4-اﻟﻒ( ﻧﻤﺎي اﻧﻮﻛﻠﺌﺎﺳﻴﻮن ﺣـﻴﻦ ﺟﺮاﺣـﻲ ﻟﻴﻮﻣﻴﻮﻣـﺎي ﻣـﺮي ،ب( ﻧﻤﻮﻧـﻪ
در %28/5ﺑﺎﻗﻲﻣﺎﻧﺪه ﺗﻮﻣﻮر در ﻣﺮي ﻣﺸﺎﻫﺪه ﻣﻲﺷﺪ .اﻳﻦ اﻓﺰاﻳﺶ ﺑﺮوز ﺗﻮﻣﻮر در ﻣﻌﺪه در ﺳﺎﻳﺮ ﻣﻄﺎﻟﻌﺎت ﻧﻴﺰ ذﻛﺮ ﺷﺪه ﺑﻮد از ﺟﻤﻠﻪ در ﻣﻄﺎﻟﻌﻪ
رزﻛﺴﻴﻮن ﺗﻮﻣﻮر ﻟﻴﻮﻣﻴﻮم ﻣﺮي
Rabinﻧﻴﺰ در %66/2از ﺑﻴﻤﺎران ﺗﻮﻣﻮر در ﻣﻌﺪه داﺷﺘﻨﺪ 16و ﻳﺎ در ﻣﻄﺎﻟﻌﻪاي ﻛﻪ Aydia Aدر ﺗﺮﻛﻴﻪ اﻧﺠﺎم داد ﻧﻴﺰ %68ﺗﻮﻣﻮرﻫﺎ در ﻣﻌﺪه ﺑﻴﻤﺎر ﻛﻪ ﻣﺘﺎﺳﺘﺎز ﻛﺒﺪي ﺑﺎ GISTﻣﻌﺪه در ﻫﻨﮕﺎم ﻣﺮاﺟﻌﻪ داﺷﺘﻪاﻧﺪ ﻓﻮت
ﮔﺰارش ﺷﺪه ﺑﻮد 2.در ﻣﻄﺎﻟﻌﻪ El-zohairyذﻛﺮ ﺷﺪه ﻛﻪ %39/4از
ﻧﻤﻮده و ﻳﻚ ﺑﻴﻤﺎر ﻣﺒﺘﻼ ﺑـﻪ ﻟﻴﻮﻣﻴﻮﺑﻼﺳـﺘﻮﻣﺎي ﻣـﺮي دو ﺳـﺎل ﺑﻌـﺪ از
ﺑﻴﻤﺎران ﻣﺒﺘﻼ ﺑﻪ ﺗﻮﻣﻮر ﻣﻌﺪه ﺑﻮدﻧﺪ اﻣﺎ ﺑﺎز ﻫﻢ ﻣﻌﺪه ﺷﺎﻳﻊﺗﺮﻳﻦ ﻣﺤﻞ 1
ﺟﺮاﺣﻲ ﺑﻪﻋﻠﺖ ﻣﺘﺎﺳﺘﺎز دوردﺳﺖ ﻓﻮت ﻧﻤﻮدﻧﺪ و ﺑﻘﻴـﻪ ﺑﻴﻤـﺎران زﻧـﺪه
اﺑﺘﻼ ﺑﻮده اﺳﺖ .ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﮔﻮارﺷﻲ ﻣﻌﻤﻮﻻً ﺑﺪون ﻋﻼﻣﺖ
ﻣﺎﻧﺪﻧﺪ %87/55 .ﺑﻴﻤﺎران ﻇﺮف ﺳﻪ ﺳﺎل ﺑﻌﺪ از درﻣﺎن زﻧﺪه ﻣﺎﻧﺪﻧﺪ.
ﻫﺴﺘﻨﺪ ﻳﺎ ﻋﻼﻳﻢ ﻏﻴﺮاﺧﺘﺼﺎﺻﻲ اﻳﺠﺎد ﻣﻲﻛﻨﻨﺪ .ﻫﺮﭼﻨﺪ ﻛﻪ در ﺑﺮﺧﻲ ﻣﻮارد ﺑﻪﺧﺼﻮص در ﻣﻮارد ﭘﻴﺸﺮﻓﺘﻪ ﺑﻴﻤﺎري ﻣﻤﻜﻦ اﺳﺖ ﻋﻼﻳﻤﻲ ﭼﻮن
ﺑﺤﺚ
ﺗﻮده ﺷﻜﻤﻲ ،درد ﺷﻜﻤﻲ ﻳﺎ ﺧﻮنرﻳﺰي ﺑﺮوز ﻛﻨﺪ 10،ﺗﻤﺎم ﺑﻴﻤﺎران در
ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل دﺳﺘﮕﺎه ﮔﻮارش از ﺑﻴﻤﺎريﻫﺎي ﻧﺎﺷﺎﻳﻊ ﻫﺴﺘﻨﺪ
زﻣﺎن ﺗﺸﺨﻴﺺ ﻋﻼﻣﺖدار ﺑﻮده ،اﻣﺎ ﺷﻜﺎﻳﺎت دﻳﮕﺮي ﭼﻮن ﻛﺎﻫﺶ
ﻛﻪ ﺑﺮوز آنﻫﺎ در ﻧﻘﺎط ﻣﺨﺘﻠﻒ دﻧﻴﺎ اﺧﺘﻼف ﭼﻨﺪاﻧﻲ ﻧﺪارد 13و ﺑﻪ
وزن ،دﻳﺴﻔﺎژي ،ﺗﻮده ﺷﻜﻤﻲ ،درد ﺷﻜﻢ و ﺗﻬﻮع و اﺳﺘﻔﺮاغ ﻧﻴﺰ در
ﮔﺮوهﻫﺎي ﻣﺨﺘﻠﻔﻲ ﺗﻘﺴﻴﻢ ﻣﻲﺷﻮﻧﺪ ﻛﻪ ﺷﺎﻣﻞ ﻟﻴﻮﻣﻴﻮم ،ﻟﻴﻮﻣﻴﻮﺳﺎرﻛﻮم،
ﺑﻴﻤﺎران ﮔﺰارش ﺷﺪه ﺑﻮد .در ﺑﻴﻦ ﺑﻴﻤﺎران ﻣﺼﺮي ﺧﻮنرﻳﺰي ﮔﻮارﺷﻲ
ﻟﻴﻮﻣﻴﻮﺑﻼﺳﺘﻮﻣﺎ و ﺷﻮاﻧﻮﻣﺎ ﻣﻲﺑﺎﺷﻨﺪ وﻟﻲ ﺷﺎﻳﻊﺗﺮﻳﻦ ﻧﻮع آنﻫﺎ ﺑﻪﻋﻨﻮان
ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻼﻣﺖ ﺑﻮد و ﻧﻴﺰ ﻓﻘﻂ %33/3از ﺑﻴﻤﺎران از ﺗﻮده ﺷﻜﻤﻲ
ﮔﺮوه
GIST
ﻃﺒﻘﻪﺑﻨﺪي ﻣﻲﺷﻮﻧﺪ .ﺗﻮﻣﻮرﻫﺎي ﮔﺮوه
GIST
ﻣﺎرﻛﺮﻫﺎي اﻳﻤﻮﻧﻮﻫﻴﺴﺘﻮﺷﻴﻤﻴﺎﻳﻲ ﺗﺸﺨﻴﺺ داده ﻣﻲﺷﻮﻧﺪ CD117
و
CD34
ﺑﺮاﺳﺎس C-Kit
و
ﺷﻜﺎﻳﺖ داﺷﺘﻨﺪ.
16
در ﮔﺰارش Berindoague Rاز ﻛﺸﻮر اﺳﭙﺎﻧﻴﺎ،
ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻼﻳﻢ آﻧﻤﻲ ) (%77و ﺧﻮنرﻳﺰي ﮔﻮارﺷﻲ ) (%68ﺑﻮده 17
در اﻳﻦ ﺗﻮﻣﻮرﻫﺎ ﻣﺜﺒﺖ اﺳﺖ .اﻳﻦ ﺑﻴﻤﺎران ﺑﻪ رژﻳﻢﻫﺎي
اﺳﺖ .در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﺗﻤﺎم ﺑﻴﻤﺎران در زﻣﺎن ﺗﺸﺨﻴﺺ ﻋﻼﻣﺖدار ﺑﻮده و
ﻣﻌﻤﻮﻟﻲ ﻛﻤﻮﺗﺮاﭘﻲ ﻣﻘﺎوم ﻫﺴﺘﻨﺪ وﻟﻲ ﭘﺎﺳﺦ ﻣﻨﺎﺳﺐ ﺑﻪ Imatinibدر
ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻼﻣﺖ ﻧﻴﺰ اﺣﺴﺎس ﭘﺮي و ﺑﻲاﺷﺘﻬﺎﻳﻲ ﺑﻮده و ﻫﻤﺎﺗﻤﺰ ﺗﻨﻬﺎ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
:Bagheriﺑﺮرﺳﻲ 24ﺑﻴﻤﺎر ﻣﺮي و ﻣﻌﺪه ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل R. et al.
442
در ﻳﻚ ﺑﻴﻤﺎر ﻣﺎ ﺑﻪﻋﻨﻮان ﻋﻼﻣﺖ ﻣﻬﻢ وﺟﻮد داﺷﺘﻪ اﺳﺖ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ
ﻧﺪاﺷﺖ و ﻋﻮارض در ﭘﻨﺞ ﺑﻴﻤﺎر ) (%20/5ﺑﻌﺪ از ﻋﻤﻞ دﻳﺪه ﺷﺪ ﻛﻪ
ﻣﺤﻞ آﻧﺎﺗﻮﻣﻴﻚ ﺿﺎﻳﻌﻪ و ﻧﻴﺰ وﺳﻌﺖ ﺿﺎﻳﻌﻪ اﻋﻤﺎل ﺟﺮاﺣﻲ ﻣﺨﺘﻠﻔﻲ در
ﺷﺎﻳﻊﺗﺮﻳﻦ آن اﻳﻠﺌﻮس ﺑﻌﺪ از ﻋﻤﻞ ﺑﻮده اﺳﺖ .در ﻣﻮرد ﻧﻘﺶ
ﺑﻴﻤﺎران اﻧﺠﺎم ﺷﺪه اﺳﺖ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺟﺎﻳﮕﺎه اﺻﻠﻲ اﻳﻦ ﺗﻮﻣﻮرﻫﺎ در
رادﻳﻮﺗﺮاﭘﻲ در اﻳﻦ ﺗﻮﻣﻮرﻫﺎ ﻧﺘﺎﻳﺞ ﻣﻮﺛﻘﻲ وﺟﻮد ﻧﺪاﺷﺘﻪ و اﻏﻠﺐ ﺑﻪ
ﻣﻌﺪه اﺳﺖ ،ﻣﻌﻤﻮﻻ ﺷﺎﻳﻊﺗﺮﻳﻦ اﻋﻤﺎل ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ ﺗﻮﺗﺎل ﻳﺎ ﺳﺎبﺗﻮﺗﺎل
رادﻳﻮﺗﺮاﭘﻲ ﻣﻘﺎوم ﻫﺴﺘﻨﺪ .ﺑﻌﺪ از ﻛﺸﻒ ﻣﻬﺎرﻛﻨﻨﺪه KITﺑﻪﻧﺎم
Imatinib
اﺳﺖ ﻛﻪ ﻧﺘﺎﻳﺞ ﻣﺘﻐﻴﺮي در ﻣﻄﺎﻟﻌﺎت ﻣﺘﻌﺪد ﺑﻴﻦ 30ﺗﺎ %35ﻛﻞ ﺑﻴﻤﺎران
ﻧﺘﺎﻳﺞ ﻣﻨﺎﺳﺒﻲ از درﻣﺎن ﺷﻴﻤﻲدرﻣﺎﻧﻲ در ﻓﺮمﻫﺎي ﻣﺘﺎﺳﺘﺎﺗﻴﻚ
18و16و2
GIST
و
در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﻧﻴﺰ ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﻤﻞ ﺟﺮاﺣﻲ ﻧﻴﺰ
ﻓﺮمﻫﺎي ﻏﻴﺮﻗﺎﺑﻞ ﺑﺮداﺷﺖ آن ﮔﺰارش ﺷﺪه اﺳﺖ ،ﺑﺎ اﻳﻦ ﺣﺎل در ﺳﺎﻳﺮ
ﺳﺎبﺗﻮﺗﺎل ﮔﺎﺳﺘﺮﻛﺘﻮﻣﻲ ﺑﻮده ﻛﻪ در %29ﺑﻴﻤﺎران اﻧﺠﺎم ﺷﺪه اﺳﺖ .از
ﻓﺮمﻫﺎي ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺜﻞ ﻟﻴﻮﻣﻴﻮﺳﺎرﻛﻮﻣﺎ و ﻟﻴﻮﻣﻴﻮﺑﻼﺳﺘﻮﻣﺎ
ﻧﻈﺮ ﺷﻴﻮع اﻧﻮاع ﭘﺎﺗﻮﻟﻮژﻳﻚ اﻳﻦ ﺗﻮﻣﻮرﻫﺎ ﻧﻴﺰ ﻣﻄﺎﻟﻌﺎت ﻣﺘﻌﺪدي اﻧﺠﺎم
اﻧﺠﺎم ﺷﻴﻤﻲدرﻣﺎﻧﻲ ﺑﺎ رژﻳﻢ ﻣﻨﺎﺳﺐ ﺑﺎ ﻳﺎ ﺑﺪون رادﻳﻮﺗﺮاﭘﻲ ﺗﻮﺻﻴﻪ
ﺷﺪه اﺳﺖ در ﻣﻄﺎﻟﻌﻪاي ﻛﻪ Yafa Wuﮔﺰارش ﻛﺮد ،ﺷﺎﻳﻊﺗﺮ ﻧﻮع
ﻣﻲﺷﻮد 20.ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ ﻛﻪ ﺑﻪدﻟﻴﻞ ﺷﻴﻮع ﻛﻢ ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل
داﻧﺴﺘﻪ ﻛﻪ اﻛﺜﺮا ﻓﺮم
ﮔﻮارﺷﻲ ﻧﺴﺒﺖ ﺑﻪﺳﺎﻳﺮ ﺗﻮﻣﻮرﻫﺎي ﮔﻮارﺷﻲ ﻧﻴﺎز ﺑﻪ ﻣﻄﺎﻟﻌﺎت ﺑﻴﺸﺘﺮ در
ﺧﻮشﺧﻴﻢ ﺑﻮدﻧﺪ ) (%57و در ﻓﺮمﻫﺎي ﺧﻮشﺧﻴﻢ ﻣﻌﻤﻮﻻ ﻋﻮد و ﺑﺮوز
اﻳﻦ زﻣﻴﻨﻪ وﺟﻮد داﺷﺘﻪ ﺑﺎﺷﺪ .ﻫﻢﭼﻨﻴﻦ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ در ﺳﺎلﻫﺎي
ﻣﺘﺎﺳﺘﺎز ﺑﻌﺪ از درﻣﺎن وﺟﻮد ﻧﺪاﺷﺖ وﻟﻲ در ﻓﺮمﻫﺎي ﺑﺪﺧﻴﻢ )(%36
اﺧﻴﺮ ﺗﺄﻛﻴﺪ روي ﭘﺎﺳﺦ درﻣﺎﻧﻲ ﺑﻪ Imatinibﺷﺪه اﺳﺖ .ﺑﺮرﺳﻲ
ﻣﻴﺰان ﻋﻮد و ﻣﺘﺎﺳﺘﺎز دوردﺳﺖ اﺳﺖ ﺑﺎﻻﺗﺮ ﺑﻮده و ﻋﻠﺖ ﻣﺮگ ﺑﻴﻤﺎران
ﻣﺎرﻛﺮﻫﺎي اﻳﻤﻮﻧﻮﻫﻴﺴﺘﻮﺷﻴﻤﻴﺎﻳﻲ ﺟﻬﺖ اﻓﺘﺮاق GISTاز ﺳﺎﻳﺮ اﻧﻮاع اﻳﻦ
ﻧﻴﺰ ﻣﺘﺎﺳﺘﺎز دوردﺳﺖ ﺑﻮده اﺳﺖ .در آن ﻣﻄﺎﻟﻌﻪ ﻧﺘﺎﻳﺞ ﭘﻴﺶآﮔﻬﻲ ﺗﻮﻣﻮر
ﺗﻮﻣﻮرﻫﺎ ﺿﺮوري ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ اﻛﺜﺮ اﻳﻦ ﺑﻴﻤﺎران
را ﺑﻪ ﺣﺠﻢ ﺗﻮﻣﻮر و ﻣﻴﺰان ﺑﺪﺧﻴﻤﻲ آن در ﺑﺮرﺳﻲ ﭘﺎﺗﻮﻟﻮژي ﻣﺮﺗﺒﻂ
ﺑﺪون ﻋﻼﻣﺖ ﻫﺴﺘﻨﺪ و ﻳﺎ ﻋﻼﻳﻢ ﻏﻴﺮاﺧﺘﺼﺎﺻﻲ ﺑﺮوز ﻣﻲدﻫﻨﺪ و
داﻧﺴﺘﻨﺪ 18.ﻧﺘﺎﻳﺞ ﻣﺸﺎﺑﻬﻲ ﻧﻴﺰ در ﻣﻄﺎﻟﻌﻪ El- Zohairyﮔﺰارش ﺷﺪه و
ﻫﻢﭼﻨﻴﻦ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻣﻜﺎن اﻧﺠﺎم اﻧﻮاع ﻣﺨﺘﻠﻒ ﺟﺮاﺣﻲﻫﺎ و درﻣﺎنﻫﺎي
وي ﻋﻮاﻣﻞ ﻣﺴﺎﻋﺪ ﭘﻴﺶآﮔﻬﻲ را رزﻛﺴﻴﻮن ﻧﺎﻛﺎﻣﻞ و درﺟﻪﺑﻨﺪي
ﺗﻜﻤﻴﻠﻲ ﺗﻮﺻﻴﻪ ﻣﻲﺷﻮد ﻛﻪ در ﻣﻮارد ﻣﺸﻜﻮك ﺑﺮرﺳﻲﻫﺎي ﺗﺸﺨﻴﺼﻲ
) (Gradingﭘﺎﺗﻮﻟﻮژي ﺗﻮﻣﻮر ذﻛﺮ ﻛﺮده اﺳﺖ 1.ﻣﻴﺰان ﻋﻮد ﻣﻮﺿﻌﻲ ﻳﺎ
دﻗﻴﻖﺗﺮ اﻧﺠﺎم ﺷﻮد .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ اﻳﻦﻛﻪ ﺟﺮاﺣﻲ در اﻳﻦ ﺑﻴﻤﺎران ﺑﺎ ﺣﺪاﻗﻞ
ﻣﺘﺎﺳﺘﺎز دوردﺳﺖ ﺑﻌﺪ از ﺟﺮاﺣﻲ و ﻣﺮگ در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﻧﻴﺰ در ﺳﻪ ﺑﻴﻤﺎر
ﻣﻮرﺑﻴﺪﻳﺘﻲ و ﻣﻮرﺗﺎﻟﻴﺘﻲ ﻫﻤﺮاه اﺳﺖ ﺑﻪﻋﻨﻮان اﺻﻠﻲﺗﺮﻳﻦ ﺑﺨﺶ درﻣﺎن
وﺟﻮد داﺷﺖ ﻛﻪ دو ﺑﻴﻤﺎر ﻣﺒﺘﻼ ﺑﻪ ﻓﺮم ﺗﻬﺎﺟﻤﻲ GISTو ﻣﺘﺎﺳﺘﺎز ﻛﺒﺪي
اﻳﻦ ﺑﻴﻤﺎران ﺗﻮﺻﻴﻪ ﻣﻲﮔﺮدد.
داﺷﺘﻪاﻧﺪ.
ﭘﺎﺗﻮﻟﻮژﻳﻚ اﻳﻦ ﺗﻮﻣﻮرﻫﺎ را در ﻣﻌﺪه
GIST
ﻫﻢزﻣﺎن ﺑﻮده و دﻳﮕﺮي ﻣﺒﺘﻼ ﺑﻪ ﻟﻴﻮﻣﻴﻮﺑﻼﺳﺘﻮﻣﺎي ﻣﺮي ﺑﻮد .در ﻣﻮرد
ﺳﭙﺎﺳﮕﺰاري :اﻳﻦ ﻣﻘﺎﻟﻪ از ﭘﺎﻳﺎنﻧﺎﻣﻪ آﻗﺎي ﻣﺤﻤﺪ ﺻﺎدق ﻓﺘﻮﻧﻲ ﺑﺎ
ﻋﻮارض و ﻣﺮگ و ﻣﻴﺮ ﺑﻌﺪ از ﺟﺮاﺣﻲ ﻧﺘﺎﻳﺞ ﻣﺘﻐﻴﺮي اﺷﺎره ﺷﺪه اﺳﺖ،
ﻣﻮﺿﻮع ﺑﺮرﺳﻲ ﺗﻮﻣﻮرﻫﺎي ﻣﺰاﻧﺸﻴﻤﺎل ﻣﺮي و ﻣﻌﺪه در ﺑﻴﻤﺎران
Braghettoﮔﺰارش ﻧﻤﻮد ﻛﻪ ﻫﻴﭻ ﻣﻮرد ﻋﺎرﺿﻪ و ﻣﺮگ و ﻣﻴﺮ ﺑﻌﺪ از
ﻣﺮاﺟﻌﻪﻛﻨﻨﺪه ﺑﻪ ﺑﻴﻤﺎرﺳﺘﺎن ﻗﺎﺋﻢ )ﻋﺞ( و اﻣﻴﺪ ﻣﺸﻬﺪ در ﻓﺎﺻﻠﻪ ﺳﺎلﻫﺎي
ﻋﻤﻞ ﻧﺪاﺷﺖ 19.در ﻣﻄﺎﻟﻌﻪ ،Eisenbergﻣﺮگ و ﻣﻴﺮ ﺑﻴﻤﺎرﺳﺘﺎﻧﻲ ﮔﺰارش
1370-86اﺳﺘﺨﺮاج ﮔﺮدﻳﺪه اﺳﺖ .ﺑﺪﻳﻦوﺳﻴﻠﻪ از ﻣﻌﺎوﻧﺖ ﭘﮋوﻫﺸﻲ
ﻧﺸﺪ ،وﻟﻲ ﻋﻮارﺿﻲ ﻣﺜﻞ ﻋﻔﻮﻧﺖ زﺧﻢ و ﺧﻮنرﻳﺰي ﮔﻮارﺷﻲ ﺑﻌﺪ از
داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﻣﺸﻬﺪ ﻛﻪ در اﻳﻦ ﭘﮋوﻫﺶ ﻧﻮﻳﺴﻨﺪﮔﺎن ﻣﻘﺎﻟﻪ را
ﻋﻤﻞ را ذﻛﺮ ﻧﻤﻮد 20.در ﻣﻄﺎﻟﻌﻪ ﻣﺎ ﻣﺮگ و ﻣﻴﺮ ﺑﻌﺪ از ﻋﻤﻞ وﺟﻮد
ﻳﺎري ﻧﻤﻮدهاﻧﺪ ،ﺻﻤﻴﻤﺎﻧﻪ ﺗﺸﻜﺮ ﻣﻲﺷﻮد.
and prognostic classification based on tumor size and MIB-1 grade. Hum Pathol 2002;33(6):669-76. 5. Staiger WI, Ronellenfitsch U, Kaehler G, Schildhaus HU, Dimitrakopoulou-Strauss A, Schwarzbach MH, et al. The Merendino procedure following preoperative imatinib mesylate for locally advanced gastrointestinal stromal tumor of the esophagogastric junction. World J Surg Oncol 2008;6:37. 6. Huang H, Liu YX, Zhan ZL, Liang H, Wang P, Ren XB. Different sites and prognoses of gastrointestinal stromal tumors of the stomach: report of 187 cases. World J Surg 2010;34(7):1523-33. 7. Burkill GJ, Badran M, Al-Muderis O, Meirion Thomas J, Judson IR, Fisher C, et al. Malignant gastrointestinal stromal tumor:
1. El-Zohairy M, Khalil el-SA, Fakhr I, El-Shahawy M, Gouda I. Gastrointestinal stromal tumor (GIST)'s surgical treatment, NCI experience. J Egypt Natl Canc Inst 2005;17(2):56-66. 2. Aydin A, Tekin F, Günşar F, Güler A, Tunçyürek M, Ilter T. Value of endoscopic ultrasonography for upper gastrointestinal stromal tumors: a single center experience. Turk J Gastroenterol 2004;15(4):233-7. 3. Divis P, Veverkova L, Capov I, Wechsler J, Zak J, Rovn I. Gastrointestinal stromal tumors- clinical experience. Scripta Med 2006;2:99-104. 4. Hasegawa T, Matsuno Y, Shimoda T, Hirohashi S. Gastrointestinal stromal tumor: consistent CD117 immunostaining for diagnosis,
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ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
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Esophagogastric mesenchymal tumors: ﻫﻤﻜﺎران وanalysis of 24 patients
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100
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Tehran University Medical Journal; Vol. 69, No. 7, October 2011: 438-444
Esophagogastric mesenchymal tumors: analysis of 24 patients
Reza Bagheri M.D.1* Ghodratolah Maddah M.D.2 Alireza Tavasoli M.D.2 Fateme Naghavi Riyabi M.D.3 1- Department of Thoracic Surgery, Endoscopic & Minimally Invasive Surgery Research Center, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 2- Department of General Surgery, Endoscopic & Minimally Invasive Surgery Research Center, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. 3- Department of General Surgery, Mashhad University of Medical Sciences, Mashhad, Iran.
Abstract
Received: January 31, 2011 Accepted: June 27, 2011
Background: Gastrointestinal mesenchymal tumors are classified as tumors that originate from smooth muscles. Gastrointestinal stromal tumors (GIST) are the most common types of the proposed tumors and can be seen in the GI tract from the esophagus to the anus, but they are mostly seen in the stomach. Mostly from the stomach and asymptomatic, the majority of patients would benefit from surgery as the best method of treatment. Methods: In this retrospective study we evaluated the data of patients with the diagnosis of esophageal or gastric mesenchymal tumors admitted in Ghaem and Omid Hospitals affiliated to Mashhad University of Medical Sciences in Iran, from 1992 to 2010. We analyzed factors such as age, sex, presenting symptoms and signs, diagnostic
methods, types of pathology, types of treatment, morbidity, mortality and 3-year survival rates. Results: Twenty four patients (16 male, 8 female) with a mean age of 50 were included in the study. The common site of tumor was gastric fundus. The most common symptom at the time of diagnosis was epigastric fullness which was observed in almost 50% of the patients. The most common type of surgery in the patients was subtotal
gastrectomy and no hospital mortality was recorded. Paralytic ileus was the commonest complication seen in five patients (20.5%). Adjuvant therapy had been performed in eight patients (33.1%). Following the patients three years postoperatively, there were only three deaths (12.45%). Conclusion: Regarding to the low mortality and morbidity of the surgeries, surgical treatment, if tolerated, is recommended for all Esophagogastric mesenchymal tumors *
Corresponding author: Endoscopic & Minimally Invasive Research Center, Ghaem Hospital, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Tel: +98-511-8012806 E-mail: Bagherir@mums.ac.ir
patients. Keywords: Complication, diagnosis, gastroesophageal, mesenchymal tumor, mortality, treatment.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
ﻛﺮوﻧﺮ 445-450 ،1390 ﻣﺪاﺧﻼت ،7ﻣﻬﺮ ، 69ﺷﻤﺎره ﻋﺮوﻗﻲدوره ﻋﻮارضﺗﻬﺮان، ﺑﺮوزﭘﺰﺷﻜﻲ داﻧﺸﮕﺎهﺑﺎﻋﻠﻮم ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜ ﭘﺲ از ﻲ ،ﻣﺮﺗﺒﻂ ﻋﻮاﻣﻞ
ﺑﺮرﺳﻲ ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﺎ ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ ﭘﺲ از ﻣﺪاﺧﻼت ﻛﺮوﻧﺮ در ﻣﺮﻛﺰ ﻗﻠﺐ و ﻋﺮوق ﺷﻬﻴﺪ رﺟﺎﻳﻲ ﺗﻬﺮان
ﺗﺎرﻳﺦ درﻳﺎﻓﺖ ﻣﻘﺎﻟﻪ 1390/03/08 :ﺗﺎرﻳﺦ ﭘﺬﻳﺮش1390/06/20 :
ﭼﻜﻴﺪه
1
اﺣﻤﺪﻋﻠﻲ ﻳﻮﺳﻔﻲ
زﻣﻴﻨﻪ و ﻫﺪف :ﻋﻮارض ﻋﺮوﻗﻲ ﺑﻪﻋﻨﻮان ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﺎرﺿﻪ آﻧﮋﻳﻮﮔﺮاﻓﻲ ﺗﺸﺨﻴﺼﻲ و آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﻋﺮوق ﻛﺮوﻧﺮ،
1
ﻣﺤﺴﻦ ﻣﻌﺪﻧﻲ
ﺑﻪﻋﻨﻮان ﻳﻚ ﻋﺎﻣﻞ ﻣﻬﻢ در ﻣﻮرﺑﻴﺪﻳﺘﻲ ﺑﻴﻤﺎران ﻣﻄﺮح ﻣﻲﺑﺎﺷﺪ و ﻟﺬا ﻣﻄﺎﻟﻌﻪ روي ﺷﻴﻮع اﻳﻦ ﻋﺎرﺿﻪ و ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﺎ
*1
ﺣﻤﻴﺪرﺿﺎ ﻋﻈﻴﻤﻲ
آن در ﺑﻴﻤﺎران ﺿﺮوري ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ .روش ﺑﺮرﺳﻲ :اﻳﻦ ﻣﻄﺎﻟﻌﻪ ،ﻳﻚ ﻣﻄﺎﻟﻌﻪ ﺗﻮﺻﻴﻔﻲ ﺑﻮده 2097 ،ﻣﻮرد
2
ﺣﺴﻴﻦ ﻓﺮﺷﻴﺪي
آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﻋﺮوق ﻛﺮوﻧﺮ در ﻣﺪت ﻳﻚﺳﺎل از ديﻣﺎه 87ﺗﺎ ديﻣﺎه 88در ﺑﻴﻤﺎرﺳﺘﺎن ﻗﻠﺐ ﺷﻬﻴﺪ رﺟﺎﻳﻲ ﺗﻬﺮان اﻧﺠﺎم -1ﮔﺮوه ﻗﻠﺐ و ﻋﺮوق ،ﺑﻴﻤﺎرﺳﺘﺎن ﻗﻠﺐ و ﻋﺮوق ﺷﻬﻴﺪ رﺟﺎﻳﻲ
ﮔﺮﻓﺖ و اﻳﻦ ﺑﻴﻤﺎران از ﻧﻈﺮ ﭘﻴﺪاﻳﺶ ﻋﻮارض ﻋﺮوﻗﻲ در ﻃﻮل ﻣﺪت ﺑﺴﺘﺮي و ﻧﻴﺰ ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﻪ آن ﻣﻮرد ﻣﻄﺎﻟﻌﻪ ﻗﺮار ﮔﺮﻓﺘﻨﺪ .ﻳﺎﻓﺘﻪﻫﺎ :از ﻛﻞ 2097ﺑﻴﻤﺎر 1544 ،ﺑﻴﻤﺎر ﻣﺬﻛﺮ ) (%73/6و 553ﺑﻴﻤﺎر ﻣﻮﻧﺚ ) (%26/4ﺑﺎ ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ
-2ﻓﻠﻮﺷﻴﭗ ﺑﺎﻟﻮن آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ،ﺑﻴﻤﺎرﺳﺘﺎن ﻗﻠﺐ و ﻋﺮوق ﺷﻬﻴﺪ رﺟﺎﻳﻲ
57±10ﺑﻮدﻧﺪ .ﻣﻴﺰان ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ از زﻣﺎن آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﺗﺎ زﻣﺎن ﺗﺮﺧﻴﺺ ﺑﻴﻤﺎر از ﺑﻴﻤﺎرﺳﺘﺎن ،در 19ﻣﻮرد ) (%0/9ﻣﺸﺎﻫﺪه ﺷﺪ ﻛﻪ از اﻳﻦ ﺗﻌﺪاد 10ﻣﻮرد ﻫﻤﺎﺗﻮم ) %52/6ﻋﻮارض( ،آﻧﻮرﻳﺴﻢ ﻛﺎذب در ﭘﻨﺞ ﻣﻮرد )%26/3
داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان.
ﻋﻮارض( ،ﺧﻮنرﻳﺰي ﺧﻠﻒ ﺻﻔﺎﻗﻲ و ﻓﻴﺴﺘﻮل ﺷﺮﻳﺎﻧﻲ ورﻳﺪي ﻫﺮ ﻛﺪام دو ﻣﻮرد ) %10/5ﻋﻮارض در ﻫﺮ ﻣﻮرد( را ﺗﺸﻜﻴﻞ دادﻧﺪ .ﻋﻮارض در ﺟﻨﺲ ﻣﻮﻧﺚ ) ،(P=0/003در ﺑﻴﻤﺎران ﺑﺎ ﺳﺎﺑﻘﻪ
HTN
) ،(P=0/02در ﺑﻴﻤﺎران ﺑﺎ ﻗﺪ ﻛﻮﺗﺎهﺗﺮ
) ،(P=0/004در ﺑﻴﻤﺎراﻧﻲ ﻛﻪ از ﻣﻬﺎرﻛﻨﻨﺪه gp IIIa/IIbاﺳﺘﻔﺎده ﻛﺮده ﺑﻮدﻧﺪ ) ،(P=0/003ﺑﻪﻃﻮر ﻗﺎﺑﻞﺗﻮﺟﻬﻲ ﺷﺎﻳﻊﺗﺮ ﺑﻮد. ﻧﺘﻴﺠﻪﮔﻴﺮي :ﻣﻴﺰان ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ در ﺑﻴﻤﺎران ﺑﻌﺪ از آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﻛﺮوﻧﺮ ﭘﺎﻳﻴﻦ اﺳﺖ و ﻳﻚ روش ﻣﻨﺎﺳﺐ درﻣﺎﻧﻲ ﺑﺮاي ﺑﻴﻤﺎران ﺑﺎ ﺗﻨﮕﻲ ﻛﺮوﻧﺮ ﻣﺤﺴﻮب ﻣﻲﺷﻮد و در ﺻﻮرﺗﻲﻛﻪ ﺑﻌﺪ از ﺑﺮداﺷﺘﻦ ﺷﻴﺖ ﺷﺮﻳﺎﻧﻲ ،در ﻣﺪت زﻣﺎن *
ﻣﻨﺎﺳﺐ ،ﻓﺸﺎر روي ﻣﺤﻞ دﺳﺘﻴﺎﺑﻲ ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﺗﻬﺮان ،ﺧﻴﺎﺑﺎن وﻟﻴﻌﺼﺮ ،اﺑﺘﺪاي ﻧﻴﺎﻳﺶ،
ﺑﻴﻤﺎرﺳﺘﺎن ﻗﻠﺐ و ﻋﺮوق ﺷﻬﻴﺪ رﺟﺎﻳﻲ
)(Access
ﻋﺮوﻗﻲ داده ﺷﻮد ،ﺑﻪﺧﺼﻮص در ﻣﻮرد ﺑﻴﻤﺎران زن ،ﺳﺎﺑﻘﻪ ،HTNﺳﻄﺢ
آﻧﺘﻲﻛﻮآﮔﻮﻻﻧﺖ ﺑﺎﻻﺗﺮ ،اﺣﺘﻤﺎل ﭘﻴﺪاﻳﺶ ﻋﻮارض ﻋﺮوق ﭘﺎﻳﻴﻦ ﻣﻲﺑﺎﺷﺪ.
ﺗﻠﻔﻦ021-23921 : E-mail: azimihamidreza66@yahoo.com
ﻛﻠﻤﺎت ﻛﻠﻴﺪي :ﻋﻮارض ﻋﺮوﻗﻲ ،ﻫﻤﺎﺗﻮم ،ﻓﻴﺴﺘﻮل ﺷﺮﻳﺎﻧﻲ ورﻳﺪي ،ﺧﻮنرﻳﺰي ﺧﻠﻒ ﺻﻔﺎﻗﻲ.
اﺳﺘﻔﺎده از ﺷﻴﺖﻫﺎي ﺷﺮﻳﺎﻧﻲ ﻛﻮﭼﻚ و وﺳﺎﻳﻞ ﻣﻜﺎﻧﻴﻜﺎل ﺑﺴﺘﻦ ﻋﺮوﻗﻲ
ﻣﻘﺪﻣﻪ
) ،(Vascular closer deviseﺳﻌﻲ در ﺟﻬﺖ ﻛﺎﻫﺶ ﻋﺎرﺿﻪ ﻋﺮوﻗﻲ
ﻣﻄﺎﻟﻌﺎت اﺧﻴﺮ ﻣﺸﺨﺺ ﻧﻤﻮده ﻛﻪ ﺧﻮنرﻳﺰي ﺑﻌﺪ از ﻛﺎﺗﺘﺮﻳﺰاﺳﻴﻮن
داﺷﺖ ،وﻟﻲ ﻫﻢﭼﻨﻴﻦ اﻳﻦ ﻋﻮارض ﺑﻪﻋﻨﻮان ﻋﺎﻣﻞ ﻣﻬﻢ در ﻣﻮرﺑﻴﺪﻳﺘﻲ
Percutaneous
ﺑﻴﻤﺎران ﻣﻄﺮح اﺳﺖ .ﺷﺮﻳﺎن ﻓﻤﻮرال ﻣﺸﺘﺮك ،ﺷﺎﻳﻊﺗﺮﻳﻦ ﻣﺤﻞ دﺳﺘﻴﺎﺑﻲ
،Coronary Interventionﺑﻪوﻳﮋه ﺧﻮنرﻳﺰي ﺧﻠﻒ ﺻﻔﺎﻗﻲ
) (Accessﻋﺮوﻗﻲ اﺳﺖ ﻛﻪ ﺑﺮاي آﻧﮋﻳﻮﮔﺮاﻓﻲ ﻛﺮوﻧﺮ ﺗﺸﺨﻴﺼﻲ و ﻧﻴﺰ
ﺑﻪﻋﻨﻮان ﻳﻚ ﻋﻠﺖ ﻗﺎﺑﻞ ﺗﻮﺟﻪ ﻣﻮرﺑﻴﺪﻳﺘﻲ و ﻣﻮرﺗﺎﻟﻴﺘﻲ ﺑﻌﺪ از اﻳﻦ
ﻣﺪاﺧﻠﻪاي ﻣﻮرد اﺳﺘﻔﺎده ﻗﺮار ﻣﻲﮔﻴﺮد .روشﻫﺎي ﺑﺮاﻛﻴﺎل و رادﻳﺎل
روشﻫﺎ ﻣﺤﺴﻮب ﻣﻲﺷﻮد .ﮔﺮﭼﻪ ﺗﻤﺎﻣﻲ ﺧﻮنرﻳﺰي ﻧﻤﻲﺗﻮاﻧﺪ ﺑﻪﻃﻮر
ﺑﻪﻋﻨﻮان روشﻫﺎي ﺟﺎﻳﮕﺰﻳﻦ ﻣﻲﺑﺎﺷﻨﺪ .ﻋﻮارض ﻣﻮﺿﻌﻲ از
1
ﻫﻤﺎﺗﻮمﻫﺎي دردﻧﺎﻛﻲ ﻛﻪ ﺧﻮدﺑﻪﺧﻮد ﺑﻬﺒﻮد ﻣﻲﻳﺎﺑﻨﺪ ﺗﺎ ﺧﻮنرﻳﺰي ﺧﻠﻒ
ﻋﻮارض ﻣﺮﺑﻮط ﺑﻪ آن ﺑﻪﻋﻨﻮان ﻳﻚ ﻋﺎﻣﻞ ﻣﻬﻢ در ﺧﻮنرﻳﺰي ﺑﻌﺪ از
ﺻﻔﺎﻗﻲ ﺗﻬﺪﻳﺪﻛﻨﻨﺪه ﺣﻴﺎت ﻣﻲﺗﻮاﻧﺪ ﻣﺘﻐﻴﺮ ﺑﺎﺷﺪ .ﺧﻮنرﻳﺰي ﺧﻠﻒ
اﻳﻦ روشﻫﺎ ﻣﻄﺮح ﻣﻲﺑﺎﺷﺪ .ﮔﺮﭼﻪ در ﺳﺎﻟﻴﺎن اﺧﻴﺮ ،ﺑﻬﺒﻮد ﺗﻜﻨﻴﻚ ،PCI
ﺻﻔﺎﻗﻲ ،اﮔﺮ Accessﺧﻴﻠﻲ ﭘﺮوﮔﺰﻳﻤﺎل ﺑﺎﺷﺪ و ﻫﻤﺎﺗﻮم ،آﻧﻮرﻳﺴﻢ
ﻗﻠﺒﻲ ﺗﺸﺨﻴﺼﻲ و ﻣﺪاﺧﻼت ﻛﺮوﻧﺮي از ﻃﺮﻳﻖ ﭘﻮﺳﺖ )(PCI
ﻣﺴﺘﻘﻴﻢ ﺑﻪﻋﻮارض در ﻣﺤﻞ دﺳﺖﻳﺎﺑﻲ ﻋﺮوﻗﻲ ﻧﺴﺒﺖ داده ﺷﻮد،
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
اﺣﻤﺪﻋﻠﻲ ﻳﻮﺳﻔﻲ و ﻫﻤﻜﺎران
446
ﻛﺎذب و ﻓﻴﺴﺘﻮل ﺷﺮﻳﺎﻧﻲ ورﻳﺪي اﮔﺮ دﺳﺘﻴﺎﺑﻲ ﺧﻴﻠﻲ دﻳﺴﺘﺎل ﺑﺎﺷﺪ
ﻣﺮگ ﺑﻪﻋﻠﺖ ﻋﻮارض ﻋﺮوﻗﻲ ،ﺧﻮنرﻳﺰي ﻋﺮوﻗﻲ ﻣﻬﻢ ) >3grاﻓﺖ
)ﻧﺴﺒﺖ ﺑﻪ ﭼﻴﻦ اﻳﻨﮕﻮﻳﻨﺎل( ،ﻣﻲﺗﻮاﻧﻨﺪ اﻳﺠﺎد ﺷﻮﻧﺪ 1-3.در اﻳﻦ ﻣﻄﺎﻟﻌﻪ در
ﺑﻪﻋﻠﺖ ﺧﻮنرﻳﺰي از ﻣﺤﻞ Accessﻳﺎ ﺧﻮنرﻳﺰي ﺧﻠﻒ ﺻﻔﺎﻗﻲ( ،ﻳﺎ از
ﻣﺪت ﻳﻚﺳﺎل ،ﻣﻴﺰان ﺑﺮوز ﻋﻮارض در ﻣﺪت ﺑﺴﺘﺮي ﺑﻴﻤﺎران ﭘﺲ از
دﺳﺖ دادن ﻧﺒﺾ ﺗﻌﺮﻳﻒ ﻣﻲﺷﺪ 2.در ﻣﻮارد ﺷﻚ ﺑﻪ ﻓﻴﺴﺘﻮل ﺷﺮﻳﺎﻧﻲ
اﻧﺠﺎم PCIو ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﺎ آن ﺑﺮرﺳﻲ ﺷﺪ .ﻋﻮارض ﺧﻮﻧﺮﻳﺰيدﻫﻨﺪه،
ورﻳﺪي ﻳﺎ آﻧﻮرﻳﺴﻢ ﻛﺎذب در ﻣﻌﺎﻳﻨﻪ ،ﺗﺸﺨﻴﺼﻲ ﺑﺎ ﺳﻮﻧﻮﮔﺮاﻓﻲ از ﻣﺤﻞ
4-7
ﺑﺎ ﺷﻴﻮع 2-6درﺻﺪ در ﻣﻄﺎﻟﻌﺎت ﻗﺒﻠﻲ ﮔﺰارش ﺷﺪه اﺳﺖ.
Hb
ﻛﺎﺗﺘﺮﻳﺴﻢ ﺗﺄﻳﻴﺪ ﻣﻲﺷﺪ و ﻧﻴﺰ در ﻣﻮارد ﺷﻚ ﺑﻪ ﺧﻮنرﻳﺰي ﺧﻠﻒ ﺻﻔﺎﻗﻲ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻋﻼﻳﻢ ﺑﺎﻟﻴﻨﻲ و ﻣﻌﺎﻳﻨﻪ ،از
CT
اﺳﻜﻦ ﻛﻤﻚ ﮔﺮﻓﺘﻪ
روش ﺑﺮرﺳﻲ
ﻣﻲﺷﺪ .در ﻧﻬﺎﻳﺖ ،اﻃﻼﻋﺎت ﻣﺮﺑﻮط ﺑﻪ ﺑﻴﻤﺎران و ﻋﺎرﺿﻪ اﻳﺠﺎد ﺷﺪه در
در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻛﻪ از ديﻣﺎه 87ﺗﺎ ديﻣﺎه 88در ﻣﺮﻛﺰ ﻗﻠﺐ و ﻋﺮوق
ﭘﺮﺳﺶﻧﺎﻣﻪ ﻣﺮﺑﻮﻃﻪ ،ﺛﺒﺖ ﮔﺮدﻳﺪ و اﻳﻦ اﻃﻼﻋﺎت ﺗﺤﻠﻴﻞ آﻣﺎري ﺷﺪ.
ﺷﻬﻴﺪ رﺟﺎﻳﻲ اﻧﺠﺎم ﺷﺪه ،ﺗﻌﺪاد 2097ﺑﻴﻤﺎر ﻛﻪ ﺗﺤﺖ PCIﻗﺮار ﮔﺮﻓﺘﻪ در ﻣﺪت ﺑﺴﺘﺮي از ﻧﻈﺮ ﭘﻴﺪاﻳﺶ ﻋﻮارض ﻋﺮوﻗﻲ ﻣﺤﻞ ﻛﺎﺗﺘﺮﻳﺰاﺳﻴﻮن،
ﻳﺎﻓﺘﻪﻫﺎ
ﻣﻮرد ﻣﻄﺎﻟﻌﻪ ﻗﺮار ﮔﺮﻓﺘﻨﺪ .ﻫﻴﭻ ﻣﻌﻴﺎري ﺟﻬﺖ ﺧﺮوج ﺑﻴﻤﺎر از ﻣﻄﺎﻟﻌﻪ
در اﻳﻦ ﻣﻄﺎﻟﻌﻪ 2097 ،ﺑﻴﻤﺎر ﺑﺮرﺳﻲ ﺷﺪﻧﺪ 1544 ،ﻧﻔﺮ ) (%73/6ﻣﺬﻛﺮ
وﺟﻮد ﻧﺪاﺷﺖ و ﻛﻠﻴﻪ ﺑﻴﻤﺎران ﻣﻮرد آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﻗﺮار ﮔﺮﻓﺘﻪ در ﻓﺎﺻﻠﻪ
و 553ﻧﻔﺮ ) (%26/4ﻣﻮﻧﺚ ﺑﻮدﻧﺪ .ﻣﻴﺎﻧﮕﻴﻦ ﺳﻨﻲ ﺑﻴﻤﺎران 57±10ﺳﺎل
زﻣﺎﻧﻲ ﻣﺬﻛﻮر ،در ﻣﻄﺎﻟﻌﻪ وارد ﺷﺪهاﻧﺪ .اﻃﻼﻋﺎت ﻣﻮرد ﻧﻴﺎز ﻃﻲ ﺗﺤﻘﻴﻖ
ﺑﻮد .در 2035ﻣﻮرد ) Access ،(%97ﻓﻤﻮرال و در 56ﻣﻮرد )،(%2/7
ﺷﺎﻣﻞ ﻳﺎﻓﺘﻪﻫﺎي دﻣﻮﮔﺮاﻓﻴﻚ و ﻣﺘﻐﻴﺮﻫﺎي ﺑﺎﻟﻴﻨﻲ ،در ﭘﺮﺳﺶﻧﺎﻣﻪ ﻣﺮﺑﻮﻃﻪ
Accessرادﻳﺎل اﺳﺘﻔﺎده ﺷﺪ .در 1359ﻣﻮرد )،(%64/8
Vascular
ﻗﺮار ﮔﺮﻓﺘﻪ و در ﻃﻲ ﻣﺪت ﺑﺴﺘﺮي ،ﺑﻴﻤﺎران از ﻧﻈﺮ ﭘﻴﺪاﻳﺶ ﻋﻮارض
Accessﺗﻮﺳﻂ ﻓﻠﻮﺷﻴﭗ آﻧﮋﻳﻮﭘﻼﺳﺘﻲ و در 732ﻣﻮرد )،(%35/2
ﻋﺮوﻗﻲ ﻣﻮرد ﻣﻌﺎﻳﻨﻪ ﻗﺮار ﻣﻲﮔﺮﻓﺘﻨﺪ .اﻧﺘﺨﺎب ﻣﺤﻞ دﺳﺖﻳﺎﺑﻲ اوﻟﻴﻪ
ﺗﻮﺳﻂ دﺳﺘﻴﺎر ﻗﻠﺐ و ﻋﺮوق ﮔﺮﻓﺘﻪ ﺷﺪه اﺳﺖ .از ﻧﻈﺮ ﻓﺮاواﻧﻲ ﻧﻮع
ﺷﺮﻳﺎن ) (Access siteﺑﻪﺗﺸﺨﻴﺺ ﭘﺰﺷﻚ ارﺷﺪ اﻧﺠﺎمدﻫﻨﺪه آﻧﮋﻳﻮﮔﺮاﻓﻲ
ﻋﺮوق ﻛﺮوﻧﺮ ﻣﻮرد آﻧﮋﻳﻮﭘﻼﺳﺘﻲ 1326 ،ﻣﻮرد ) (%63/2ﻣﺮﺑﻮط ﺑﻪ
ﺻﻮرت ﻣﻲﮔﺮﻓﺖ .روش ارﺟﺢ دﺳﺘﻴﺎﺑﻲ ﻓﻤﻮرال ﺑﻮد و دﺳﺘﻴﺎﺑﻲ رادﻳﺎل
576 ،LADﻣﻮرد ) ،(%27/5ﻣﺮﺑﻮط ﺑﻪ ﺷﺮﻳﺎن ﺳﻴﺮﻛﻤﻔﻠﻜﺲ ﭼﭗ
در ﻣﻮاردي ﻛﻪ دﺳﺘﻴﺎﺑﻲ ﻓﻤﻮرال ﻗﺎﺑﻞ دﺳﺘﺮﺳﻲ ﻧﺒﻮد ،ﺑﻪﻋﻨﻮان روش
) (LCXو 689ﻣﻮرد ) (%32/9ﻣﺮﺑﻮط ﺑﻪ ﺷﺮﻳﺎن ﻛﺮوﻧﺮي راﺳﺖ
Right
ﺟﺎﻳﮕﺰﻳﻦ اﻧﺠﺎم ﻣﻲﺷﺪ .ﻛﻠﻴﻪ ﺑﻴﻤﺎران ﻗﺒﻞ از ورود ﺑﻪﺑﺨﺶ آﻧﮋﻳﻮﮔﺮاﻓﻲ
) Coronary Artery (RCAﺑﻮده اﺳﺖ .ﻻزم ﺑﻪذﻛﺮ اﺳﺖ ﻛﻪ در ﺗﻌﺪادي
ASA
) 80-325ﻣﻴﻠﻲﮔﺮم روزاﻧﻪ( و ﭘﻼوﻳﻜﺲ ) 300-600ﮔﺮم
از ﺑﻴﻤﺎران دو ﻳﺎ ﺳﻪ رگ ﺑﻪﻃﻮر ﻫﻢزﻣﺎن ﻣﻮرد
PCI
ﻗﺮار ﮔﺮﻓﺘﻨﺪ.
ﺑﻪﺻﻮرت دوز اﺑﺘﺪاﻳﻲ و 75ﻣﻴﻠﻲﮔﺮم روزاﻧﻪ( درﻳﺎﻓﺖ ﻛﺮده ﺑﻮدﻧﺪ.
ﻫﻤﺎنﮔﻮﻧﻪ ﻛﻪ در ﺟﺪول 1ﻣﻼﺣﻈﻪ ﻣﻲﺷﻮد ،اﻛﺜﺮ ﺑﻴﻤﺎران )،(%81
وﻳﺮاﺳﺖ ﭘﺎﻧﺰدﻫﻢ
LVEFﻧﺮﻣﺎل ﻳﺎ اﺧﺘﻼل ﻋﻤﻠﻜﺮدي ﺧﻔﻴﻒ ) (Mild dysfunctionداﺷﺘﻨﺪ
ﻣﻮرد ﺗﺠﺰﻳﻪ و ﺗﺤﻠﻴﻞ آﻣﺎري ﻗﺮار ﮔﺮﻓﺘﻪ و ارﺗﺒﺎط ﻣﺘﻐﻴﺮﻫﺎي ﻣﺨﺘﻠﻒ و
و ﻧﺎرﺳﺎﻳﻲ ﻣﺘﻮﺳﻂ ﺗﺎ ﺷﺪﻳﺪ ﺑﻄﻦ ﭼﭗ در ﻛﻢﺗﺮ از %20ﺑﻴﻤﺎران وﺟﻮد
ﻣﻴﺰان ﺗﺄﺛﻴﺮ آن ﺑﺮ ﺷﻴﻮع ﻋﻮارض ﻋﺮوﻗﻲ ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار ﮔﺮﻓﺖ.
داﺷﺖ .از ﻧﻈﺮ ﻧﻮع ﺷﻴﺖ ) (Sheatﺑﻪﻛﺎر رﻓﺘﻪ ،در 863ﻣﻮرد )،(%41/2
Fisher’s exact
،6Fدر 1225ﻣﻮرد ) 7F ،(%58/5و در ﭘﻨﺞ ﻣﻮرد )(%0/2؛ 8Fدر
testو Student’s t-testاﺳﺘﻔﺎده ﺷﺪ .ﺑﺮ اﺳﺎس اﻳﻦ ﻣﻄﺎﻟﻌﻪ ،ﻫﻴﭻ
ﺑﻴﻤﺎران اﺳﺘﻔﺎده ﺷﺪ .ﺟﺪول ،2وﺿﻌﻴﺖ ﻛﺎرﻛﺮد ﻛﻠﻴﻪ ﺑﻴﻤﺎران را ﺑﺮ
داروﻳﻲ ﺧﺎرج از ﺑﺮﻧﺎﻣﻪ ﻣﻌﻤﻮل آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﺑﻪ ﺑﻴﻤﺎر ﺗﺠﻮﻳﺰ ﻧﺸﺪه و
اﺳﺎس ﻋﺪد ﻛﺮاﺗﻲﻧﻴﻦ ﺳﺮم در روز اﻧﺠﺎم آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﻛﺮوﻧﺮ ﻧﺸﺎن
ﻫﺰﻳﻨﻪ ﻣﺎﻟﻲ اﺿﺎﻓﻲ ﺑﻪ ﺑﻴﻤﺎر ﺗﺤﻤﻴﻞ ﻧﮕﺮدﻳﺪه ،ﺗﻤﺎم ﺑﻴﻤﺎران از روال
ﻣﻲدﻫﺪ .اﻟﺒﺘﻪ ﻻزم ﺑﻪذﻛﺮ اﺳﺖ ﻛﻪ ﻋﺪد ﻛﺮاﺗﻲﻧﻴﻦ ﺳﺮم ﺷﺎﺧﺺ ﻗﺎﺑﻞ
اﻧﺠﺎم ﻓﻌﺎﻟﻴﺖ ﻣﻌﻤﻮل ﺑﺨﺶ ﺧﺎرج ﻧﺸﺪﻧﺪ .ﻋﻮارض اﻳﺠﺎد ﺷﺪه در
اﻃﻤﻴﻨﺎﻧﻲ ﺑﺮاي ﺑﺮرﺳﻲ وﺿﻌﻴﺖ ﻛﻠﻴﻪ ﺑﻴﻤﺎران ﻧﺒﻮده و ﺑﻬﺘﺮ اﺳﺖ ﻛﻪ از
ﻳﺎﻓﺘﻪﻫﺎي ﭘﺮﺳﺶﻧﺎﻣﻪ ﺑﺎ اﺳﺘﻔﺎده از ﻧﺮماﻓﺰار
SPSS
ﺑﺮاي ﺗﺠﺰﻳﻪ و ﺗﺤﻠﻴﻞ اﻃﻼﻋﺎت از آزﻣﻮنﻫﺎي
2
و
ﺑﻴﻤﺎران ،ﺑﺮ اﺳﺎس ﺗﻌﺎرﻳﻒ American college of cardiologyﺑﺮاي
ﻣﺤﺎﺳﺒﻪ ﻣﻴﺰان ﻓﻴﻠﺘﺮاﺳﻴﻮن ﮔﻠﻮﻣﺮوﻟﻲ
ﻋﻮارض ﻋﺮوﻗﻲ ﺗﻌﺮﻳﻒ ﻣﻲﺷﺪ 2.ﻋﻮارض ﻋﺮوﻗﻲ ﺧﻔﻴﻒ ﺑﻪﻋﻨﻮان ﻫﺮ
ﺷﻮد ،وﻟﻲ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺣﺠﻢ ﻧﻤﻮﻧﻪ زﻳﺎد ،اﻣﻜﺎن اﻳﻦ ﻣﺤﺎﺳﺒﻪ ﻣﻴﺴﺮ ﻧﺸﺪ
ﻛﺪام از ﻣﻮارد زﻳﺮ ﺗﻌﺮﻳﻒ ﻣﻲﺷﺪﻧﺪ :ﻫﻤﺎﺗﻮم< 10ﺳﺎﻧﺘﻲﻣﺘﺮ ،ﻓﻴﺴﺘﻮل
و ﻣﺎ ﺑﻪ اﻧﺪازهﮔﻴﺮي Crﺳﺮم ﺑﻪﻋﻨﻮان ﺗﺨﻤﻴﻨﻲ از وﺿﻌﻴﺖ ﻛﻠﻴﻪ ﺑﻴﻤﺎران
ﺷﺮﻳﺎﻧﻲ ورﻳﺪي ،ﻳﺎ آﻧﻮرﻳﺴﻢ ﻛﺎذب ،ﻋﻮارض ﻋﺮوﻗﻲ ﻋﻤﺪه ﺑﻪﺻﻮرت
ﺑﺴﻨﺪه ﻛﺮدﻳﻢ .در ﻋﻴﻦ ﺣﺎل ﻫﻤﺎنﮔﻮﻧﻪ ﻛﻪ ﻣﻼﺣﻈﻪ ﻣﻲﮔﺮدد ،ﻧﺰدﻳﻚ ﺑﻪ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
)(GFR
ﺑﺮاي اﻳﻦ ﻣﻨﻈﻮر اﺳﺘﻔﺎده
447
ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﺎ ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ ﭘﺲ از ﻣﺪاﺧﻼت ﻛﺮوﻧﺮ
ﺟﺪول :1-ﻓﺮاواﻧﻲ ﺑﻴﻤﺎران ﺑﺮ اﺳﺎس ﻣﻴﺰان ﻛﺎرﻛﺮد ﻋﻀﻠﻪ ﺑﻄﻦ ﭼﭗ
)(LVEF
ﺟﺪول :2-ﻓﺮاواﻧﻲ ﺑﻴﻤﺎران ﺑﺮ اﺳﺎس ﻣﻴﺰان ﻛﺮاﺗﻲﻧﻴﻦ ﺳﺮم
LVEF
ﺗﻌﺪاد
درﺻﺪ
Crﺳﺮم )(mg/dl
ﺗﻌﺪاد
درﺻﺪ
<%30
121
%5/8
<1
488
%23/4
%30-%39
273
%13/1
1-1/5
1373
%65/8
%40-%49
821
%39/5
1/5-2
179
%8/6
≥%50
866
%41/6
>2
47
%2/3
ﻧﻤﻮدار :1-ﻓﺮاواﻧﻲ ﻋﻮارض ﻣﺨﺘﻠﻒ ﻋﺮوﻗﻲ
ﻧﻤﻮدار :3-ﺑﺮرﺳﻲ ﺳﺎﺑﻘﻪ ﻫﻴﭙﺮﺗﺎﻧﺴﻴﻮن ﺑﺮ ﭘﻴﺪاﻳﺶ ﻋﻮارض ﻋﺮوﻗﻲ
ﻧﻤﻮدار :2-ﻣﻘﺎﻳﺴﻪ ﺟﻨﺴﻲ ﭘﻴﺪاﻳﺶ ﻋﻮارض ﻋﺮوﻗﻲ
ﻧﻤﻮدار :4-ﺑﺮرﺳﻲ اﺛﺮ gp IIIa/IIb inh.ﺑﺮ ﭘﻴﺪاﻳﺶ ﻋﻮارض ﻋﺮوﻗﻲ
%90ﺑﻴﻤﺎران Cr ،ﻛﻢﺗﺮ از 1/5دارﻧﺪ .ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻋﺎرﺿﻪ ﻣﺴﻤﻮﻣﻴﺖ
ﻋﻮارض( ،آﻧﻮرﻳﺴﻢ ﻛﺎذب در ﭘﻨﺞ ﻣﻮرد ) %26/3ﻋﻮارض( ،ﺧﻮنرﻳﺰي
ﻛﻠﻴﻮي ﺷﻨﺎﺧﺘﻪ ﺷﺪه ﻣﻮاد ﺣﺎﺟﺐ در آﻧﮋﻳﻮﮔﺮاﻓﻲ و آﻧﮋﻳﻮﭘﻼﺳﺘﻲ
ﺧﻠﻒ ﺻﻔﺎﻗﻲ و ﻓﻴﺴﺘﻮل ﺷﺮﻳﺎﻧﻲ ورﻳﺪي ﻫﺮ ﻛﺪام در دو ﻣﻮرد )در ﻫﺮ
ﻛﺮوﻧﺮ ،ﺑﻪﻃﻮر ﻣﻌﻤﻮل ،در ﺑﻴﻤﺎراﻧﻲ ﻛﻪ Crﺑﺎﻻ دارﻧﺪ ،ﻓﻘﻂ در ﺷﺮاﻳﻂ
ﻣﻮرد %10/5ﻋﻮارض( وﺟﻮد داﺷﺖ )ﻧﻤﻮدار .(1ﻓﻘﻂ ﻫﻤﺎﺗﻮم ﻗﺎﺑﻞ
ﺧﺎص ﻛﻪ ﻣﻴﺰان ﻓﺎﻳﺪه ﺑﻪﺧﻄﺮ اﻧﺠﺎم آﻧﮋﻳﻮﮔﺮاﻓﻲ ﻗﺎﺑﻞ ﻗﺒﻮل ﺑﺎﺷﺪ ،اﻳﻦ
ﺗﻮﺟﻪ ،ﻳﻌﻨﻲ ﻫﻤﺎﺗﻮﻣﻲ ﻛﻪ ﺑﻴﺶ از ﺷﺶ ﺳﺎﻧﺘﻲﻣﺘﺮ ﻗﻄﺮ داﺷﺘﻪ و ﻳﺎ ﺑﺎ
ﻛﺎر ﺑﺎ اﺣﺘﻴﺎط ﺧﺎص ﺻﻮرت ﻣﻲﮔﻴﺮد .ﻣﻴﺰان ﻋﻮارض ﻋﺮوﻗﻲ از زﻣﺎن
اﻓﺖ ﻫﻤﻮﮔﻠﻮﺑﻴﻦ ﺑﻴﺶ ﻳﺎ ﻣﺴﺎوي 3g/dlﻫﻤﺮاه ﺑﻮد در ﻣﻄﺎﻟﻌﻪ ﻣﻨﻈﻮر
اﻧﺠﺎم آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ﺗﺎ زﻣﺎن ﺗﺮﺧﻴﺺ ﺑﻴﻤﺎر از ﺑﻴﻤﺎرﺳﺘﺎن ،در 19ﻣﻮرد
ﺷﺪ و ﻫﻤﺎﺗﻮمﻫﺎي ﻛﻮﭼﻚ ﺑﻪﻋﻨﻮان ﻋﺎرﺿﻪ در ﻧﻈﺮ ﮔﺮﻓﺘﻪ ﻧﺸﺪه اﺳﺖ.
) (%0/9ﻣﺸـﺎﻫﺪه ﺷـﺪ ﻛـﻪ از اﻳـﻦ ﺗﻌـﺪاد 10ﻣـﻮرد ﻫﻤـﺎﺗﻮم )%52/6
ارﺗﺒﺎط ﻋﻮارض ﺑﺎ ﻣﺘﻐﻴـﺮﻫﺎي ﻣﺨﺘﻠﻒ :ﻋﻮارض ﻋﺮوﻗﻲ ،ﺑﻪﻃﻮر ﻗﺎﺑﻞ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
اﺣﻤﺪﻋﻠﻲ ﻳﻮﺳﻔﻲ و ﻫﻤﻜﺎران
448
ﻛﺎﺗﺘﺮ 7Fﻛﻢﺗﺮ ﺑﻮد وﻟـﻲ اﺧـﺘﻼف ﻣﻌﻨـﻲداري ﻧﺪاﺷـﺖ ) .(P=0/82در
ﺟﺪول :3-ﻣﻘﺎﻳﺴﻪ ﺑﻴﻤﺎران داراي ﻋﺎرﺿﻪ ﻋﺮوﻗﻲ و ﺑﺪون آن ﻋﺎرﺿﻪ ﻋﺮوﻗﻲ
ﺑﺪون ﻋﺎرﺿﻪ ﻋﺮوﻗﻲ
ﺧﺼﻮﺻﻴﺎت
)(n=19
)(n=2078
ﺳﻦ )ﺳﺎل(
57/812
57/410
*0/87
ﺟﻨﺲ زن
%57/9
%26/1
**0/003
دﻳﺎﺑﺖ
%42/1
%27/9
**0/19
ﺳﻴﮕﺎر
%26/3
%40/4
**0/24
ﻫﻴﭙﺮﻟﻴﭙﻴﺪﻣﻲ
%47/4
%40/2
**0/63
ﻫﻴﭙﺮﺗﺎﻧﺴﻴﻮن
%68/4
%43/7
**0/03
ﻧﺎرﺳﺎﻳﻲ ﻛﻠﻴﻪ
%15/8
%10/7
**0/17
27/044
28/63/9
**0/07
BMI
P
ﻣﻘﺎﻳﺴﻪ اﺧﺘﻼف ﺷﻴﻮع ﻋﻮارض ﻋﺮوﻗـﻲ در ﺑﻴﻤـﺎراﻧﻲ ﻛـﻪ دﺳـﺖﻳـﺎﺑﻲ ﻋﺮوﻗﻲ ﺗﻮﺳـﻂ رزﻳـﺪﻧﺖ ﻳـﺎ ﻓﻠـﻮي Interventionﮔﺮﻓﺘـﻪ ﺷـﺪه ﺑـﻮد، اﺧﺘﻼف ﻣﻌﻨﻲداري ﻣﺸﺎﻫﺪه ﻧﺸﺪ ) .(P=0/13در ﻣﻮرد ﻋﺎرﺿـﻪ ﻋﺮوﻗـﻲ ﺧﺎص در ﻃﻮل اﻧﺠﺎم PCIﻫﻤﺎﺗﻮم در ﺑﻴﻤﺎران ﺟﻨﺲ ﻣﺆﻧﺚ )(P=0/005 و ﻗﺪ ﻛﻮﺗﺎه ﺗﺮ ) (P=0/009ﺷﺎﻳﻊ ﺗﺮ ﺑـﻮد .ﻓﻴـﺴﺘﻮل ﺷـﺮﻳﺎﻧﻲ ورﻳـﺪي در BMIﺑﺎﻻﺗﺮ ) (P=0/02و در ﺑﻴﻤﺎران ﺑﺎ وزن ﺑﻴﺶﺗﺮ ) (P=0/05ﺷـﺎﻳﻊﺗـﺮ ﺑﻮد .ﺧﻮنرﻳﺰي ﺧﻠـﻒ ﺻـﻔﺎﻗﻲ در ﺑﻴﻤـﺎران ﺑـﺎ ﺳـﻦ ﭘـﺎﻳﻴﻦﺗـﺮ ﺷـﻴﻮع ﺑﻴﺶﺗﺮي داﺷﺖ ) .(P=0/02آﻧﻮرﻳﺴﻢ ﻛﺎذب ﺷـﺮﻳﺎﻧﻲ در ﺑﻴﻤـﺎراﻧﻲ ﻛـﻪ ﻣﻬﺎرﻛﻨﻨﺪه gp IIIa/IIbاﺳﺘﻔﺎده ﺷﺪه ﺑﻮد ،ﺷﺎﻳﻊﺗﺮ ﺑﻮد ).(P=0/01
اﻧﺪﻳﻜﺎﺳﻴﻮن آﻧﮋﻳﻮﭘﻼﺳﺘﻲ ) STEMIﻃﻲ 7روز(
%26/3
%28/9
**0/51
ﺑﺤﺚ
Chronic CAO
%31/6
%43/5
**0/35
در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ،ﻋﻮارض ﻋﺮوﻗﻲ در 0/9درﺻﺪ ﺑﻴﻤﺎران ﻣﺸﺎﻫﺪه ﺷﺪ.
UA/NSTEMI
%10/5
%8/1
**0/66
ﻫﻤﺎﺗﻮم ﻣﻮﺿﻌﻲ در ﻣﺤﻞ ﻛﺸﺎﻟﻪ ران ،ﺑﻪﻋﻨﻮان ﺷﺎﻳﻊﺗﺮﻳﻦ ﻋﺎرﺿﻪ
<%40
%26/4
%18/9
%40-49
%26/3
%39/6
>%50
%47/4
%41/5
**0/47
%21/1
%3/1
**0/003
162/19/1
167/78/3
*0/004
ﻋﺮوﻗﻲ ﻣﺤﺴﻮب ﻣﻲﺷﻮد .ﻣﺎ ﻋﻮاﻣﻞ ﻣﺮﺑﻮط ﺑﻪ ﺑﻴﻤﺎر و ﻧﻮع ﻣﺪاﺧﻠﻪ
LVEF
ﻣﻬﺎرﻛﻨﻨﺪه ﻗﺪ
gp IIIa/IIb
P<0/05ﻣﻌﻨﻲدار * آزﻣﻮن آﻣﺎري ** ،t-testآزﻣﻮن آﻣﺎري
) (Procedureرا ﻛﻪ روي ﻣﻴﺰان ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ ﻣﺆﺛﺮﻧﺪ ،ﺑﺮرﺳﻲ ﻧﻤﻮدﻳﻢ .ﻋﻮاﻣﻞ ﻣﺮﺑﻮط ﺑﻪ ﺑﻴﻤﺎر ﺷﺎﻣﻞ ﺟﻨﺲ زن ،ﺳﺎﺑﻘﻪ ،HTNﻗﺪ
Fisher’s exact test
BMI: Body Mass Index, STEMI: ST Elevation MI, CAD: Coronary Artery Disease, UA/NSTEMI: Unstable Angina/ Non ST Elevation MI, LVEF: LV Ejection Fraction
ﻛﻮﺗﺎهﺗﺮ و BMIﺑﺎﻻﺗﺮ ﺑﻮد ،در اﺳﺘﻔﺎده از داروي ﻣﻬﺎر ﻛﻨﻨﺪه
gp IIIa/IIb
ﻫﻨﮕﺎم ،PCIﻣﻴﺰان ﺑﺮوز ﻋﻮارض ﻋﺮوﻗﻲ ﺑﻪﻃﻮر ﻗﺎﺑﻞ ﺗﻮﺟﻬﻲ ﺷﺎﻳﻊﺗﺮ ﺑﻮد .ﻣﻄﺎﻟﻌﺎت ﻣﺘﻌﺪدي ،ﻋﻮاﻣﻞ ﻫﻤﺮاه ﺑﺎ اﻓﺰاﻳﺶ ﺧﻄﺮ اﻳﺠﺎد ﻋﻮارض ﻋﺮوﻗﻲ ﻫﻨﮕﺎم آﻧﮋﻳﻮﮔﺮاﻓﻲ ﻛﺮوﻧﺮ و
PCI
را ﻣﺸﺨﺺ ﻧﻤﻮدهاﻧﺪ .ﺟﻨﺲ
زن ،ﻋﻤﻞ اورژاﻧﺲ ،ﺳﺎﻳﺰ Sheatو ﻧﺎرﺳﺎﻳﻲ ﻛﻠﻴﻪ ،ﭘﻴﺶﮔﻮﻳﻲﻛﻨﻨﺪهﻫﺎي ﻣﺴﺘﻘﻞ اﻓﺰاﻳﺶ ﻋﻮارض ﻋﺮوﻗﻲ ﺑﻮدهاﻧﺪ 8.ﺟﻨﺲ زن ،ﻋﻤﻞ اورژاﻧﺲ و
ﺗﻮﺟﻬﻲ در ﺟﻨﺲ ﻣﺆﻧﺚ )) (P=0/003ﻧﻤﻮدار ،(2در ﺑﻴﻤﺎران ﺑـﺎ ﺳـﺎﺑﻘﻪ
Access siteﺷﺮﻳﺎن ﻓﻤﻮرال در ﻣﺤﻞ ﺷﺮﻳﺎن اﭘﻲﮔﺎﺳﺘﺮﻳﻚ ﺗﺤﺘﺎﻧﻲ ﻳﺎ 9
) (P=0/027) HTNﻧﻤﻮدار ،(3در ﺑﻴﻤﺎران ﺑﺎ ﻗﺪ ﻛﻮﺗـﺎه ﺗـﺮ )،(P=0/004
ﺑﺎﻻي آن ،ﻫﻤﺮاه ﺑﺎ اﻓﺰاﻳﺶ ﺧﻮنرﻳﺰي ﺧﻠﻒ ﺻﻔﺎﻗﻲ ﻣﻲﺑﺎﺷﺪ .ﻣﺎ
gp IIIa/IIb
ﻫﻢﭼﻨﻴﻦ ﻣﻴﺰان اﻳﺠﺎد ﻋﻮارض ﻋﺮوﻗﻲ را ﻧﺴﺒﺖ ﺑﻪ ﺳﺎﻳﺰ Sheatﻣﻮرد
اﺳﺘﻔﺎده ﺷﺪه ﺑﻮد )) (P=0/003ﻧﻤﻮدار (4ﺷﺎﻳﻊﺗﺮ ﺑﻮد .وﺿـﻌﻴﺖ ﺑـﺎﻟﻴﻨﻲ
اﺳﺘﻔﺎده ،ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار دادﻳﻢ .ﮔﺮﭼﻪ ﻋﻮارض ﻋﺮوﻗﻲ در ﺳﺎﻳﺰ 7F
NSTEMI ،UA ،Chronicو (STEMI
ﺷﺎﻳﻊﺗﺮ از ﺳﺎﻳﺰ 6Fﺑﻮد ،وﻟﻲ ارﺗﺒﺎط ﻗﺎﺑﻞ ﺗﻮﺟﻪ و آﻣﺎري ﻣﻌﻨﻲداري
در ﺑﻴﻤــﺎراﻧﻲ ﻛــﻪ در ﻃــﻮل اﻧﺠــﺎم ،PCIداروي ﻣﻬﺎرﻛﻨﻨــﺪه ﺑﻴﻤﺎران در زﻣـﺎن ﻣﺮاﺟﻌـﻪ
)CAD
PCI
از ﻃﺮﻳﻖ ﺷﺮﻳﺎن رادﻳﺎل در اﻳﻦ ﻣﻄﺎﻟﻌﻪ،
ﺗﺎﺛﻴﺮي روي ﺷﻴﻮع ﻋﻮارض ﻧﺪاﺷﺖ .ﺷﻴﻮع ﻋﻮارض ﻋﺮوﻗﻲ ،ﺑـﺎ ﻣﻴـﺰان
دﻳﺪه ﻧﺸﺪ .ﺗﻌﺪاد ﻣﻮارد
ﻛﺎرﻛﺮد ﻋﻀﻠﻪ ﻗﻠﺒﻲ ﺑﻴﻤﺎران ) ،(P=0/47) ،(LVEFﺑﺎ ﻣﻴﺰان ﻛﺎرﻛﺮد ﻛﻠﻴـﻪ
ﺧﻴﻠﻲ ﻛﻢ ﺑﻮد و ﻋﻠﻲرﻏﻢ اﻳﻦﻛﻪ ﻣﺎ ﻫﻴﭻ ﻋﺎرﺿﻪ ﻋﺮوﻗﻲ ﺑﺎ روش رادﻳﺎل
ﺑﻴﻤﺎران ) ،(P=0/17ﺷﺎﺧﺺ ﺗﻮده ﺑﺪﻧﻲ ) ،(P=0/07) (BMIﺳﻦ ﺑﻴﻤـﺎران
ﻧﺪاﺷﺘﻴﻢ ،وﻟﻲ ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﺗﻌﺪاد ﺧﻴﻠﻲ ﻛﻢ ﻣﻮارد ﻧﺴﺒﺖ ﺑﻪ ﺷﺮﻳﺎن
) ،(P=0/87ﻓــﺸﺎر ﺧــﻮن ﺳﻴــﺴﺘﻮﻟﻴﻚ و دﻳﺎﺳــﺘﻮﻟﻴﻚ در روز اﻧﺠــﺎم
ﻓﻤﻮرال ،ﻣﻘﺎﻳﺴﻪ ارزﺷﻤﻨﺪي ﻣﺤﺴﻮب ﻧﻤﻲﺷﻮد .ﺷﻴﻮع ﻋﺎرﺿﻪ ﻋﺮوﻗﻲ
آﻧﮋﻳﻮﭘﻼﺳــﺘﻲ و وزن ﺑﻴﻤــﺎران ارﺗﺒــﺎط ﻣﻌﻨــﻲداري ﻧﺪاﺷــﺖ .ﻋــﻮارض
ﺑﻌﺪ از ،PCIدر اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﭘﺎﻳﻴﻦ ﺑﻮد ) 0/9درﺻﺪ( ،اﻳﻦ ﺷﻴﻮع ﭘﺎﻳﻴﻦﺗﺮ
ﻋﺮوﻗﻲ در ﺑﻴﻤﺎراﻧﻲ ﻛﻪ ﻛﺎﺗﺘﺮ 6Fاﺳﺘﻔﺎده ﺷﺪه ﺑﻮد ،ﻧﺴﺒﺖ ﺑﻪ ﺑﻴﻤﺎران ﺑـﺎ
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ، 69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
از ﺷﻴﻮع ﮔﺰارشﺷﺪه در ﻣﻄﺎﻟﻌﺎت ﻗﺒﻠﻲ ﻣﻲﺑﺎﺷﺪ )ﺣﺪود 1/5درﺻﺪ(،
10
ﭘﺲ از ﻣﺪاﺧﻼت ﻛﺮوﻧﺮ ﻋﺮوﻗﻲA.A. ﻋﻮارض ﻋﻮاﻣﻞ ﻣﺮﺗﺒﻂ ﺑﺎ ﺑﺮوز Yousefi et al.
449
روي ﺷﺮﻳﺎن در ﻣﺪت زﻣﺎن ﻣﻨﺎﺳﺐ ﻓﺸﺎر ﻻزم ﺑﺎ دﺳﺖ اﻋﻤﺎل،ﺷﺮﻳﺎﻧﻲ
ﺷﺎﻳﺪ اﻳﻦ ﺗﻔﺎوت ﺑﻪﻋﻠﺖ ﻃﻴﻒ ﺗﻌﺮﻳﻒ ﺑﺎرﻳﻚﺗﺮ ﻋﻮارض ﻋﺮوﻗﻲ اﺳﺖ
اﻳﻦ. اﺣﺘﻤﺎل ﭘﻴﺪاﻳﺶ ﻋﻮارض در اﻳﻦ ﻣﺤﻞ ﺑﺴﻴﺎر ﻛﻢ ﺧﻮاﻫﺪ ﺑﻮد،ﺷﻮد
ﻣﺎ ﻋﻮارض ﻋﺮوﻗﻲ را ﺑﻌﺪ، اﻟﺒﺘﻪ.ﻛﻪ در اﻳﻦ ﻣﻄﺎﻟﻌﻪ اﺳﺘﻔﺎده ﺷﺪه اﺳﺖ
ﻣﻄﺎﻟﻌﻪ، ﻳﻚ ﺑﺮرﺳﻲ ﺗﻚ ﻣﺮﻛﺰي ﺑﻮده و ﺑﺮاي ارزﻳﺎﺑﻲ ﺟﺎﻣﻊﺗﺮ،ﻣﻄﺎﻟﻌﻪ
ﭼﺮا ﻛﻪ ﺑﻌﻀﻲ از ﻋﻮارض،از ﺗﺮﺧﻴﺺ از ﺑﻴﻤﺎرﺳﺘﺎن ارزﻳﺎﺑﻲ ﻧﻜﺮدﻳﻢ
ﭼﻨﺪ ﻣﺮﻛﺰي در ﺑﻴﻤﺎرﺳﺘﺎنﻫﺎي ﻣﺨﺘﻠﻒ ﺑﺎ ﺗﻌﺪاد ﻣﻮارد ﺑﻴﺶﺗﺮ ﺗﻮﺻﻴﻪ
ﻣﺜﻞ ﻓﻴﺴﺘﻮل ﺷﺮﻳﺎﻧﻲ ورﻳﺪي ﻳﺎ آﻧﻮرﻳﺴﻢ ﻛﺎذب ﻣﻤﻜﻦ اﺳﺖ ﺑﻪﺻﻮرت
ﺑﺎ ﺗﻮﺟﻪ ﺑﻪاﺣﺘﻤﺎل ﭘﻴﺪاﻳﺶ ﺑﻌﻀﻲ ﻋﻮارض ﻋﺮوﻗﻲ ﺑﻪﺻﻮرت.ﻣﻲﺷﻮد
ﻳﺎﻓﺘﻪﻫﺎي اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﻣﺸﺨﺺ ﻣﻲﻛﻨﺪ ﻛﻪ اﻧﺠﺎم.ﺗﺄﺧﻴﺮي ﻇﺎﻫﺮ ﺷﻮﻧﺪ
ﭘﺎﻳﺶ ﺑﻴﻤﺎران در روزﻫﺎي ﺑﻌﺪ آﻧﮋﻳﻮﮔﺮاﻓﻲ ﻧﻴﺰ ﺟﻬﺖ،ﺗﺄﺧﻴﺮي
از ﻃﺮﻳﻖ ﺷﺮﻳﺎن ﻓﻤﻮرال ﻳﻚ روش ﻛﻢﻋﺎرﺿﻪ از ﻧﻈﺮ ﭘﻴﺪاﻳﺶ
.ﻣﺸﺨﺺ ﻧﻤﻮدن دﻗﻴﻖﺗﺮ ﺗﻌﺪاد ﻋﻮارض ﻋﺮوﻗﻲ ﭘﻴﺸﻨﻬﺎد ﻣﻲﺷﻮد
PCI
ﻋﻮارض ﻋﺮوﻗﻲ ﻣﻲﺑﺎﺷﺪ و در ﺻﻮرﺗﻲﻛﻪ در ﻣﺤﻞ ﺧﺎرج ﻛﺮدن وﺳﻴﻠﻪ
References 1. Topol EJ, editor. Textbook of Interventional Cardiology. 5th ed. Philadelphia, PA: WB Saunders; 2008. p. 513-28. 2. Eeckhout E, Carlier S, Lerman A, Kern M, editors. Handbook of Complications During Percutaneous Coronary Interventions. London: Taylor and Francis: Informa Healthcare; 2007. p. 53-62. 3. Libby P, Bonow R, Mann D, Zipes D, editors. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Philadelphia, PA: WB Saunders; 2008. p. 1423-4. 4. Applegate RJ, Sacrinty MT, Kutcher MA, Kahl FR, Gandhi SK, Santos RM, et al. Trends in vascular complications after diagnostic cardiac catheterization and percutaneous coronary intervention via the femoral artery, 1998 to 2007. JACC Cardiovasc Interv 2008;1(3):317-26. 5. Piper WD, Malenka DJ, Ryan TJ Jr, Shubrooks SJ Jr, O'Connor GT, Robb JF, et al. Predicting vascular complications in percutaneous coronary interventions. Am Heart J 2003;145(6):1022-9. 6. Dumont CJ, Keeling AW, Bourguignon C, Sarembock IJ, Turner M. Predictors of vascular complications post diagnostic cardiac
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
catheterization and percutaneous coronary interventions. Dimens Crit Care Nurs 2006;25(3):137-42. 7. Kelm M, Perings SM, Jax T, Lauer T, Schoebel FC, Heintzen MP, et al. Incidence and clinical outcome of iatrogenic femoral arteriovenous fistulas: implications for risk stratification and treatment. J Am Coll Cardiol 2002;40(2):291-7. 8. Tavris DR, Dey S, Albrecht-Gallauresi B, Brindis RG, Shaw R, Weintraub W, et al. Risk of local adverse events following cardiac catheterization by hemostasis device use - phase II. J Invasive Cardiol 2005;17(12):644-50. 9. Farouque HM, Tremmel JA, Raissi Shabari F, Aggarwal M, Fearon WF, Ng MK, et al. Risk factors for the development of retroperitoneal hematoma after percutaneous coronary intervention in the era of glycoprotein IIb/IIIa inhibitors and vascular closure devices. J Am Coll Cardiol 2005;45(3):363-8. 10. Koreny M, Riedmüller E, Nikfardjam M, Siostrzonek P, Müllner M. Arterial puncture closing devices compared with standard manual compression after cardiac catheterization: systematic review and meta-analysis. JAMA 2004;291(3):350-7.
Tehran University Medical Journal;ﻫﻤﻜﺎران Vol. 69, وNo. 7, October 2011: 445-450
100
The factors relevant to the onset of vascular complications after coronary intervention in Shahid Rajaei Cardiovascular Center in Tehran, Iran
1
Ahmad Ali Yousefi M.D. Mohsen Madani M.D.1 Hamid Reza Azimi M.D.1* Hossein Farshidi M.D.2 1- Department of Cardiovascular, Shahid Rajaei Hospital, Tehran University of Medical Sciences, Tehran, Iran. 2- Fellowship of Angioplasty, Department of Cardiovascular, Shahid Rajaei Hospital, Tehran University of Medical Sciences, Tehran, Iran.
Abstract
Received: May 29, 2011 Accepted: September 11, 2011
Background: Vascular complications, as the most common complications of diagnostic catheterization and percutaneous coronary intervention (PCI), are important factors in the morbidity of patients undergoing such procedures; thus, this study was done to evaluate the prevalence of these complications and their related factors. Methods: This is a descriptive study composed of 2097 consecutive patients who underwent percutaneous coronary intervention in Shahid Rajaei Cardiovascular Center in Tehran, Iran from January 2008 to January 2009. Occurrence of vascular complications in course of hospitalization and the related factors leading to the complications were investigated. Results: Out of 2097 patients, 1544 (73.6%) were male and 553 (26.4%) were female, and the mean age of the participants was 5710 years. Vascular complications from the time of PCI to the time discharge were observed in 19 (0.9%) patients. The other complications included: hematoma in 10 cases (52.6%), pseudoaneurysm in five cases (26.3%), retroperitoneal hemorrhage and arteriovenous fistula in 2 (10.5%) patients each.
The complications were significantly more common in female patients (P=0.003), in patients with a history of hypertension (P=0.02), people of shorter stature (P=0.004), and being on gp IIIa/IIb inhibitors (P=0.003). Conclusion: The rate of vascular complications post-percutaneous coronary interventions is low and it is considered to be a good treatment option for patients with coronary stenosis; provided that sufficient compression is applied on the vascular access point in the right time after removal of the arterial sheath. PCI is of fewer vascular complications, especially in female patients, history of hypertension, and higher anticoagulant concentrations. *
Corresponding author: Shahid Rajaei Hospital, Next to Mellat Park, Valiasr St., Tehran, Iran. Tel: +98-21-23921 E-mail: azimihamidreza66@yahoo.com
Keywords: Arteriovenous fistula, hematoma, hemorrhage, retroperitoneal, vascular complication.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
ﻣﻮش ﺳﺮم ،در ﻟﻴﭙﻴﺪﻫﺎي ﺷﻤﺎرهو ﻛﻮرﺗﻴﺰول ﺗﻴﺮوﻳﻴﺪ، ﻫﻮرﻣﻮن ﻣﺎﻳﻜﺮووﻳﻮ اﺟﺎق 451 1390 ﺷﻤﺎره،7،4ﺗﻴﺮﻣﻬﺮ ،69 ﺗﻬﺮان، ﭘﺰﺷﻲﻜﻲ ﻋﻠﻮم داﻧﺸﮕﺎه ﻲ،ﻲ، ﭘﺰﺷﻜ ﺪهﺪه ﻧﺸﺘﻲﻜ داﻧﺸ ﻣﺠﻠﻪ 312 ،1390 دوره، 69 دوره ﺗﻬﺮان، وزن،ﭘﺰﺷﻜ ﺑﺮﻋﻠﻮم داﻧﺸﮕﺎه ﭘﺰﺷﻜ اﻣﻮاجداﻧﺸﻜ ﺗﺎﺛﻴﺮﻣﺠﻠﻪ
آﺗﺮزي ﻛﻮآن :ﺗﺠﺮﺑﻪ 13ﺳﺎﻟﻪ و ﺑﺮرﺳﻲ ﻣﺘﻮن :ﮔﺰارش ﻛﻮﺗﺎه
آﺗﺮزي ﻛﻮآن ) (Choanal atresiaﻛﻪ اﺑﺘﺪا ﺗﻮﺳﻂ دﻛﺘﺮ Roederدر
ﻋﻼﻳﻤﻲ از اﻧﺴﺪاد ﺑﻴﻨﻲ ﻣﺮاﺟﻌﻪ ﻛﺮده ﻛﻪ در ﺑﻴﻦ آنﻫﺎ %18ﻣﻮارد
ﺳﺎل 1755ﻣﻌﺮﻓﻲ ﺷﺪ 1،ﺑﺎرﻳﻚ ﺷﺪن ﻳﺎ اﻧﺴﺪاد دﻫﺎﻧﻪ ﺧﻠﻔﻲ ﺣﻔﺮه ﺑﻴﻨﻲ
دوﻃﺮﻓﻪ و ﺑﺎ ﺳﻴﺎﻧﻮز ﻫﻤﺮاه ﺑﻮده اﺳﺖ و %64ﻣﻮارد ﻧﻴﺰ رﻳﻨﻮره داﺷﺘﻨﺪ.
اﺳﺖ .اﻳﻦ ﺑﻴﻤﺎري ﻣﻲﺗﻮاﻧﺪ ﻣﺎدرزادي ﻳﺎ اﻛﺘﺴﺎﺑﻲ رخ دﻫﺪ .اﻏﻠﺐ
ﻣﻴﺎﻧﮕﻴﻦ ﺑﻴﻤﺎران ﻣﺎ 12/4ﺳﺎل ﻣﺤﺎﺳﺒﻪ ﺷﺪ ﻛﻪ ﻧﺴﺒﺖ ﺑﻪ ﻣﻄﺎﻟﻌﺎت دﻳﮕﺮ
ﻣﺒﺘﻼﻳﺎن ﺑﻪ اﻳﻦ ﺑﻴﻤﺎري ﻣﻮﻧﺚ ﻫﺴﺘﻨﺪ 2.ﻣﻮارد ﻣﺎدرزادي ﻣﻤﻜﻦ اﺳﺖ
ﻛﻤﻲ ﺑﺎﻻﺗﺮ اﺳﺖ و اﻳﻦ ﻣﺴﺌﻠﻪ ﻣﻲﺗﻮاﻧﺪ ﻧﺎﺷﻲ از ﻣﺮاﺟﻌﻪ دﻳﺮﻫﻨﮕﺎم و
اﻳﺰوﻟﻪ ﺑﻮده ﻳﺎ ﻫﻤﺮاه ﺑﺎ ﻧﺎﻫﻨﺠﺎريﻫﺎي دﻳﮕﺮي ﻧﻈﻴﺮ ﻫﻤﺮاﻫﻲ ﺳﻨﺪرم
ﻋﺪم آﮔﺎﻫﻲ ﺑﻴﻤﺎران از ﻋﻼﻳﻢ و ﻛﻤﺒﻮد ﻣﺮاﻛﺰ ﺑﻬﺪاﺷﺘﻲ در ﺳﻄﺢ ﻛﺸﻮر
ﺑﺎﺷﻨﺪ ﻛﻪ اﻳﻦ ﻣﻮارد ﺣﺪود %20-50از ﻣﻮارد ﻣﺎدرزادي را
ﺑﺎﺷﺪ .روش ﺗﺮاﻧﺲ ﭘﺎﻻﺗﺎل ﺑﻴﺶﺗﺮﻳﻦ روش ﻣﻮرد اﺳﺘﻔﺎده ﺗﺎ اواﺧﺮ دﻫﻪ
CHARGE
3
ﺗﺸﻜﻴﻞ ﻣﻲدﻫﻨﺪ .آﺗﺮزي ﻛﻮان ﻣﻲﺗﻮاﻧﺪ ﻳﻚﻃﺮﻓﻪ ﻳﺎ دوﻃﺮﻓﻪ ﺑﺎﺷﺪ؛ ﺑﺎ
80ﺑﻮده اﺳﺖ .اﻳﻦ روش ﺑﻪﻋﻠﺖ ﺗﻮاﻧﺎﻳﻲ اﻳﺠﺎد ورودي اﺑﺘﺪاﻳﻲ
وﺟﻮد اﻳﻦﻛﻪ ﻣﻮارد دوﻃﺮﻓﻪ ﺟﺪيﺗﺮ ﺑﻮده و ﻧﻴﺎزﻣﻨﺪ درﻣﺎن اورژاﻧﺲ
ﺑﺰرگﺗﺮ دﺳﺘﺮﺳﻲ ﻣﻨﺎﺳﺐﺗﺮي را ﻓﺮاﻫﻢ ﻣﻲﻛﻨﺪ .اﻣﺎ در دو دﻫﻪ اﺧﻴﺮ
ﻫﺴﺘﻨﺪ ،ﻣﻮارد ﻳﻚﻃﺮﻓﻪ ﺷﺎﻳﻊﺗﺮ ﺑﻮده و اﻛﺜﺮا ﺳﻤﺖ راﺳﺖ را درﮔﻴﺮ
روش ﺗﺮاﻧﺲ ﻧﺎزال ارﺟﺢ ﺑﻮده اﺳﺖ .در اﻳﻦ روش ﺑﺎ اﺳﺘﻔﺎده از
ﻣﻲﻧﻤﺎﻳﻨﺪ .آﺗﺮزي ﻛﻮان ﻣﻲﺗﻮاﻧﺪ ﻣﻨﺸﺎ اﺳﺘﺨﻮاﻧﻲ ،ﻏﺸﺎﻳﻲ ﻳﺎ ﻣﺨﺘﻠﻂ
آﻧﺪوﺳﻜﻮپ ﻣﻲﺗﻮان ﻣﻜﺎن دﻗﻴﻖ رزﻛﺴﻴﻮن را ﺗﻌﻴﻴﻦ و اﻣﻨﻴﺖ ﺟﺮاﺣﻲ
داﺷﺘﻪ ﺑﺎﺷﺪ 2.در ﺣﺎل ﺣﺎﺿﺮ درﻣﺎن ﻗﻄﻌﻲ آﺗﺮزي ﻛﻮان ،درﻣﺎن ﺟﺮاﺣﻲ
را اﻓﺰاﻳﺶ داد 4.اﺳﺘﻔﺎده از اﺳﺘﻨﺖ در ﺟﺮاﺣﻲ آﺗﺮزي ﻛﻮان ﻫﻨﻮز ﻣﻮرد
اﺳﺖ .در ﺣﺎل ﺣﺎﺿﺮ ،ﺳﻪ روش ﺟﺮاﺣﻲ ﺗﺮاﻧﺲ ﭘﺎﻻﺗﺎل ،ﺗﺮاﻧﺲ ﺳﭙﺘﺎل
ﺑﺤﺚ اﺳﺖ .ﺑﻌﻀﻲ ﻧﻮﻳﺴﻨﺪﮔﺎن ﻋﻘﻴﺪه دارﻧﺪ اﺳﺘﻨﺖ ﻣﺎﻧﻊ ﺗﻨﮕﻲ ﻣﺠﺪد
و ﺗﺮاﻧﺲ ﻧﺎزال )ﺑﻪوﺳﻴﻠﻪ آﻧﺪوﺳﻜﻮپ( ارﺟﺢ ﻫﺴﺘﻨﺪ 3.در اﻳﻦ ﭘﮋوﻫﺶ
ﻣﻲﺷﻮد در ﺣﺎﻟﻲﻛﻪ ﺑﻌﻀﻲ دﻳﮕﺮ ﺑﻪ اﻓﺰاﻳﺶ رﻳﺴﻚ ﻋﻔﻮﻧﺖ و اﺳﻜﺎر ﺑﺎ
ﭘﺮوﻧﺪه ﺗﻤﺎﻣﻲ ﺑﻴﻤﺎراﻧﻲ ﻛﻪ از ﺳﺎل 1376ﺗﺎ ﺳﺎل 1388ﺑﻪ ﺑﻴﻤﺎرﺳﺘﺎن
اﺳﺘﻔﺎده از اﺳﺘﻨﺖ ﻣﻌﺘﻘﺪﻧﺪ 5.ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻣﻮارد ذﻛﺮ ﺷﺪه ﺑﺮرﺳﻲﻫﺎي
اﻣﻴﺮاﻋﻠﻢ ﻣﺮاﺟﻌﻪ ﻧﻤﻮدهاﻧﺪ ﻣﻄﺎﻟﻌﻪ ﺷﺪ .ﺑﺎ ﺟﺴﺘﺠﻮ در ﺑﺨﺶ ﺑﺎﻳﮕﺎﻧﻲ
ﺑﻴﺸﺘﺮ در زﻣﻴﻨﻪ آﺗﺮزي ﻛﻮان ،ﺑﻬﺘﺮﻳﻦ روشﻫﺎي ﺟﺮاﺣﻲ و ﺗﻜﻨﻴﻚﻫﺎﻳﻲ
ﺑﻴﻤﺎرﺳﺘﺎن اﻣﻴﺮاﻋﻠﻢ 54ﺑﻴﻤﺎر ﻣﻮرد آﺗﺮزي ﻛﻮان ﻛﻪ در اﻳﻦ ﺑﻴﻤﺎرﺳﺘﺎن
ﺟﻬﺖ ﺗﺸﺨﻴﺺ زودرس آن ﺿﺮوري ﺑﻪﻧﻈﺮ ﻣﻲرﺳﺪ.
ﺗﺤﺖ ﻋﻤﻞ ﺟﺮاﺣﻲ ﻗﺮار ﮔﺮﻓﺘﻨﺪ ﻳﺎﻓﺖ ﺷﺪ .ﺳﻦ اﻳﻦ ﺑﻴﻤﺎران از دو ﺗﺎ 29ﺳﺎل ﻣﺘﻐﻴﺮ و ﻣﻴﺎﻧﮕﻴﻦ و ﻣﻴﺎﻧﻪ ﺳﻦ ﺑﻴﻤﺎران ﺑﻪﺗﺮﺗﻴﺐ 12/4و 12 ﺳﺎل ﺑﻮد .ﻧﺴﺒﺖ دﺧﺘﺮ ﺑﻪ ﭘﺴﺮ دو ﺑﻪ ﻳﻚ ﺑﻮده و ﻧﺴﺒﺖ ﻣﻮارد ﻳﻚﻃﺮﻓﻪ ﺑﻪ دوﻃﺮﻓﻪ 1/9: 1ﻣﺤﺎﺳﺒﻪ ﺷﺪ .از ﺑﻴﻦ ﻣﻮارد ﻳﻚﻃﺮﻓﻪ 19ﻣﻮرد ﺳﻤﺖ
*
ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﻣﺤﺴﻦ ﻧﺮاﻗﻲ ،ﮔﺮوه ﮔﻮش ،ﮔﻠﻮ ،ﺑﻴﻨﻲ و ﺟﺮاﺣﻲ
ﺳﺮ و ﮔﺮدن ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان. ﻧﺎزﻧﻴﻦ ﺣﺠﺮاﻻﺳﻮدي ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان.
راﺳﺖ ﺑﻮدﻧﺪ 40 .ﻣﻮرد ﻣﺨﺘﻠﻂ 13 ،ﻣﻮرد اﺳﺘﺨﻮاﻧﻲ ﺑﻮدﻧﺪ و ﻳﻚ ﻣﻮرد
* ﺷﻤﺎره ﺗﻠﻔﻦ021-66703037 :
ﻧﻴﺰ ﻏﺸﺎﻳﻲ ﻣﺸﺎﻫﺪه ﺷﺪ .ﭘﻨﺞ ﺑﻴﻤﺎر از ﻃﺮﻳﻖ ﺗﺮاﻧﺲ ﭘﺎﻻﺗﺎل و ﺑﻘﻴﻪ ﻣﻮارد
آدرس :ﺗﻬﺮان ،ﺧﻴﺎﺑﺎن ﺳﻌﺪي ،ﺑﻴﻤﺎرﺳﺘﺎن اﻣﻴﺮاﻋﻠﻢ ،ﮔﺮوه ﮔﻮش ،ﮔﻠﻮ ،ﺑﻴﻨﻲ و ﺟﺮاﺣﻲ
ﺗﺤﺖ روش آﻧﺪوﺳﻜﻮﭘﻴﻚ ﺑﺪون اﺳﺘﻨﺖ ﺟﺮاﺣﻲ ﺷﺪﻧﺪ %80 .ﻣﻮارد ﺑﺎ
ﺳﺮ و ﮔﺮدن
E-mail: naraghim@sina.tums.ac.ir
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ،69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
452 ،1390 ﻣﻬﺮ،7 ﻫﻤﻜﺎرانﺷﻤﺎره ،69 ودوره،ﺗﻬﺮان داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜ،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ﻏﻼﻣﻌﻠﻲﻲﺟﻠﻮدار
The choanal atresia: 13- year experience and a review of the literature: brief report
Choanal atresia was first described by Roeder in 1755.1 Choanal atresia is the narrowing or obstruction of the posterior nasal fossa. This anomaly could be congenital or acquired. Most patients are female.2 Choanal atresia might be isolated or associated with other anomalies like CHARGE syndrome and 20-50% of congenital cases have this company.3 Choanal atresia could be unilateral or bilateral; while bilateral cases are emergent surgical conditions, unilateral cases are more frequent and mostly right-sided. Choanal atresia may be osseous, membranous or mixed.2 The definite treatment for choanal atresia is surgery and transpalatal, transseptal and transnasal (with endoscope) are the three preferable approaches.3 The medical records of fifty-four patients diagnosed with choanal atresia and admitted in Amiralam university hospital during the years 1998 to 2010 were evaluated. The patients were 2 to 29 years old with a mean and median age of 12.4 and 12, respectively. Female to male ratio was 2:1 and unilateral to bilateral involvement ratio was 1.9:1. Among unilateral cases, 19 cases had right-sided involvement. Forty cases had mixed, 13 had osseous, and one of them had membranous choanal atresia. Five patients had undergone transplatal surgery and the rest had their choanal atresia repaired by endoscopic approach. 80% of the cases had revisited for symptoms of nasal obstruction among which 18% had bilateral obstruction and presented with cyanosis and 64% had rhinorrhea. In comparison to similar studies, our patients had a higher mean age. This could be due to late referral, the patients’ unfamiliarity with the symptoms and inadequacy of specialized treatment centers. Transpalatal approach was the most common surgical approach till late 80s as it provided better access due to the provision of a wider opening. Providing direct access to the surgical field and causing the least trauma to the site, endoscopic approach has been the most preferable option during the last two decades. In this approach, the exact site of resection can be determined and surgical safety will be increased.4 Use of stents in the surgery of choanal atresia is still controversial. Some authors believe in the prevention of recurrence with stents while some think about higher probability of infection and scar.5 Regarding the mentioned issues above, more research is needed to find the best surgical approaches and techniques for the early detection and treatment of choanal atresia. *
Corresponding author: Mohsen Naraghi M.D.
Department of Otorhinolaryngology, Head and Neck Surgery, Tehran University of Medical
Sciences, Tehran, Iran.
Nazanin HajarolAsvadi M.D. Tehran University of Medical Sciences, Tehran, Iran. * Address: Amiralam Hospital, Sa’di St., Enghelab Ave., Tehran, Iran. Tel: +98-21-66703037 E-mail: naraghim@sina.tums.ac.ir
References 1. Ramsden JD, Campisi P, Forte V. Choanal atresia and choanal stenosis. Otolaryngol Clin North Am 2009;42(2):339-52, x. 2. da Fontoura Rey Bergonse G, Carneiro AF, Vassoler TM. Choanal atresia: analysis of 16 cases: the experience of HRAC-USP from 2000 to 2004. Braz J Otorhinolaryngol 2005;71(6):730-3. 3. Hengerer AS, Brickman TM, Jeyakumar A. Choanal atresia: embryologic analysis and evolution of treatment, a 30-year experience. Laryngoscope 2008;118(5):862-6.
4. Assanasen P, Metheetrairut C. Choanal atresia. J Med Assoc Thai 2009;92(5):699-706. 5. Mantovani M, Mosca F, Laguardia M, Di Cicco M, Pignataro L. A new dynamic endonasal stent for bilateral congenital choanal atresia. Acta Otorhinolaryngol Ital 2009;29(4):209-12
1390 ﻣﻬﺮ،7 ﺷﻤﺎره،69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
ﻣﻮش ﺳﺮم ،در ﻛﻮرﺗﻴﺰول و ﺗﻴﺮوﻳﻴﺪ، ﻣﺎﻳﻜﺮووﻳﻮ اﺟﺎق 453 ﻟﻴﭙﻴﺪﻫﺎي1390 ﺷﻤﺎره ،7ﻣﻬﺮ دوره ،69 ﻫﻮرﻣﻮنﺗﻬﺮان، وزن ،ﭘﺰﺷﻜﻲ ﺑﺮ ﻋﻠﻮم داﻧﺸﮕﺎه ﭘﺰﺷﻜﻲ، ﻧﺸﺘﻲﻜﺪه اﻣﻮاج داﻧﺸ ﺗﺎﺛﻴﺮ ﻣﺠﻠﻪ
اﻧﺴﻴﺪاﻧﺲ ﺳﻨﺪروم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ ﺑﻌﺪ از ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ﺑﺎ ﻟﻴﺪوﻛﺎﻳﻴﻦ و ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ :ﺗﺎﺛﻴﺮ ﻧﻮع ﺳﻮزن و ﭘﻮزﻳﺸﻦ ﺟﺮاﺣﻲ :ﮔﺰارش ﻛﻮﺗﺎه
ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ
)(TNS
ﺑﻪﺻﻮرت ﻛﻤﺮ درد ﻳﺎ درد در
ﺑﻴﻤﺎر درد در ﻧﺎﺣﻴﻪ ﻟﻮﻣﺒﻮﺳﺎﻛﺮال ﺑﺎ اﻧﺘﺸﺎر ﺑﻪ اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺑﻮد ﻛﻪ ﺑﺎ
ﻧﺎﺣﻴﻪ ﺑﺎﺳﻦ و اﻧﺪام ﺗﺤﺘﺎﻧﻲ ﺑﻮده و ﻣﻌﻤﻮﻻ ﻣﻮﻗﺘﻲ ﻣﻲﺑﺎﺷﺪ .اﻳﻦ ﺳﻨﺪرم
ﻧﺸﺴﺘﻦ ﺗﺸﺪﻳﺪ ﻣﻲﻳﺎﻓﺖ و در 22ﻣﻮرد درد در ﻧﺎﺣﻴﻪ ران ﺑﻮد .دردﻫﺎ
اوﻟﻴﻦﺑﺎر ﺗﻮﺳﻂ Schneiderدر ﺳﺎل 1993ﮔﺰارش ﮔﺮدﻳﺪه و ﺑﻪﻧﺎم
ﺑﻪﻃﻮر ﻋﻤﺪه 6-8ﺳﺎﻋﺖ ﺑﻌﺪ از اﺳﭙﺎﻳﻨﺎل ﺷﺮوع ﻣﻲﺷﺪ .ﻣﺘﻮﺳﻂ درد
اﻧﺴﻴﺪاﻧﺲ ﺳﻨﺪروم
ﺑﻴﻤﺎران ﺑﺮﺣﺴﺐ ) Visual Analog Scale (VASﺷﺶ ﺑﻮد ﻛﻪ ﺑﺎ داروي
ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ ﺑﻌﺪ از ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ﺑﺎ ﻟﻴﺪوﻛﺎﻳﻴﻦ %10 ،ﺗﺎ %40
ﭘﺘﺪﻳﻦ ﻛﺎﻫﺶ ﻣﻲﻳﺎﻓﺖ .از ﻧﻈﺮ ﻧﻮع ﺳﻮزن اﺳﭙﺎﻳﻨﺎل اﺧﺘﻼف واﺿﺤﻲ
ﻫﺪف اوﻟﻴﻪ اﻳﻦ ﻣﻄﺎﻟﻌﻪ ﺗﻌﻴﻴﻦ درﺻﺪ ﺑﺮوز
ﺑﻴﻦ دو ﻧﻮع ﺳﻮزن ،در ﺑﺮوز ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ وﺟﻮد ﻧﺪاﺷﺖ
2و1
ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ ﻧﺎﻣﻴﺪه ﺷﺪ. 4و3
ﮔﺰارش ﺷﺪه اﺳﺖ.
ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ در اﻳﻦ ﺑﻴﻤﺎران و ﻫﺪف ﺛﺎﻧﻮﻳﻪ ﺗﻌﻴﻴﻦ ارﺗﺒﺎط
).(P=0/7
ﺑﺮوز ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ ﺑﺎ ﻧﻮع ﺳﻮزن ﻳﺎ ﻧﻮع ﭘﻮزﻳﺸﻦ ﺟﺮاﺣﻲ
در اﻳﻦ ﻣﻄﺎﻟﻌﻪ ،اﻧﺴﻴﺪاﻧﺲ ﻋﻮارض ﻧﻮروﻟﻮژﻳﻚ ﺑﺎ ﻟﻴﺪوﻛﺎﻳﻴﻦ ﺑﻴﺸﺘﺮ از
ﺑﻮده اﺳﺖ .اﻳﻦ ﻣﻄﺎﻟﻌﻪ آﻳﻨﺪهﻧﮕﺮ ﺑﺮ روي 250ﺑﻴﻤﺎر
)(ASA I-II
در
5
ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ﺑﻮد ﻛﻪ اﻳﻦ ﻳﺎﻓﺘﻪ ﺑﺎ ﻣﻄﺎﻟﻌﻪ Keldﻫﻢﺧﻮاﻧﻲ دارد.
ﻣﺤﺪوده ﺳﻨﻲ 18ﺗﺎ 60ﺳﺎل ﻛﻪ ﻛﺎﻧﺪﻳﺪاي ﺟﺮاﺣﻲ در دو ﭘﻮزﻳﺸﻦ
در ﭘﻮزﻳﺸﻦ Supineﺑﺮوز ﻛﻤﺮدرد ﺑﺴﻴﺎر ﻛﻤﺘﺮ ﺑﻮد ،ﺷﺎﻳﺪ ﻋﻠﺖ آن اﻳﻦ
ﻟﻴﺘﻮﺗﻮﻣﻲ و ﺳﻮﭘﺎﻳﻦ ﺑﻮدﻧﺪ ﻃﺮاﺣﻲ ﮔﺮدﻳﺪ .ﺑﻴﻤﺎران ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻧﻮع
ﺑﺎﺷﺪ ﻛﻪ در وﺿﻌﻴﺖ ﺳﻮﭘﺎﻳﻦ ﺳﺘﻮن ﻓﻘﺮات ﻛﻤﺮي ﺣﺎﻟﺖ ﻟﻮردوز
ﺳﻮزن اﺳﭙﺎﻳﻨﺎل ) (Sprotte or Quinckeو ﻧﻮع داروي ﺑﻲﺣﺴﻲ
ﻃﺒﻴﻌﻲ ﺧﻮد را ﺣﻔﻆ ﻣﻲﻛﻨﺪ وﻟﻲ در وﺿﻌﻴﺖ ﻟﻴﺘﻮﺗﻮﻣﻲ ﻟﻮردوز ﻛﻤﺮي
) (Lidocaine or bupivacaineﺑﻪﻃﻮر ﺗﺼﺎدﻓﻲ ﺑﻪ ﭼﻬﺎر ﮔﺮوه ﺗﻘﺴﻴﻢ
ﻛﺎﻫﺶ ﻳﺎﻓﺘﻪ و ﺣﺎﻟﺖ ﺻﺎف ﭘﻴﺪا ﻣﻲﻛﻨﺪ .در اﻳﻦ وﺿﻌﻴﺖ ﻋﻀﻼت،
ﺷﺪﻧﺪ .ﻫﻤﻪ ﺑﻴﻤﺎران ﺑﻌﺪ از اﻧﺠﺎم ﻣﺎﻧﻴﺘﻮرﻳﻨﮓ اﺳﺘﺎﻧﺪارد ﺗﻮﺳﻂ
ﺗﺎﻧﺪونﻫﺎ ،ﻣﻔﺎﺻﻞ و اﻋﺼﺎب دماﺳﺒﻲ ﻛﺸﻴﺪﮔﻲ ﻳﺎﻓﺘﻪ و اﺣﺘﻤﺎل ﺑﺮوز
ﻣﺘﺨﺼﺺ ﺑﻴﻬﻮﺷﻲ در ﺳﻄﺢ L2- L3ﻳﺎ L3- L4ﺗﺤﺖ ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل
ﻛﻤﺮدرد اﻓﺰاﻳﺶ ﻣﻲﻳﺎﺑﺪ .ﻧﻮروﺗﻮﻛﺴﻴﺴﻴﺘﻪ ﻟﻴﺪوﻛﺎﻳﻴﻦ در ﻣﻘﺎﻳﺴﻪ ﺑﺎ
ﻗﺮار ﮔﺮﻓﺘﻨﺪ .ﺑﻌﺪ از ﺑﻲﺣﺴﻲ اﺳﭙﺎﻳﻨﺎل ﺑﻴﻤﺎران ﺑﺎ ﺗﻮﺟﻪ ﺑﻪ ﻧﻮع ﺟﺮاﺣﻲ،
ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ﺑﻴﺸﺘﺮ اﺳﺖ ﻛﻪ ﺷﺎﻳﺪ ﻳﻜﻲ از ﻋﻠﻞ اﻓﺰاﻳﺶ ﺑﺮوز
در وﺿﻌﻴﺖ ﺳﻮﭘﺎﻳﻦ ﻳﺎ ﻟﻴﺘﻮﺗﻮﻣﻲ ﻗﺮار ﮔﺮﻓﺘﻨﺪ .در ﻃﻲ ﺳﻪ روز ﺑﻌﺪ از
ﮔﺮوه ﻟﻴﺪوﻛﺎﻳﻴﻦ ﺑﺎﺷﺪ.
ﻋﻤﻞ ﺟﺮاﺣﻲ ﺑﻴﻤﺎران از ﻧﻈﺮ ﺑﺮوز
)(TNS
)(TNS
در
ﻣﻮرد ﺑﺮرﺳﻲ ﻗﺮار ﮔﺮﻓﺘﻨﺪ.
ﻫﺮﮔﻮﻧﻪ درد و ﻛﺮﺧﺘﻲ ﻳﺎ ﻫﻴﭙﺮآﻟﮋزي در ﻧﺎﺣﻴﻪ ﻛﻤﺮ ،ﺑﺎﺳﻦ ،ﻗﺴﻤﺖ ﻗﺪاﻣﻲ ﻳﺎ ﺧﻠﻔﻲ ران ،زاﻧﻮ ،ﺳﺎق و ﭘﺎﻫﺎ ﺑﻪﺻﻮرت ﻳﻚﻃﺮﻓﻪ ﻳﺎ دوﻃﺮﻓﻪ ﺛﺒﺖ ﮔﺮدﻳﺪ .ﻫﻤﻴﻦﻃﻮر ﺧﺼﻮﺻﻴﺎت درد ﻣﺎﻧﻨﺪ اﺣﺴﺎس ﺳﻮزش ،اﻧﺘﺸﺎر درد ،ارﺗﺒﺎط درد ﺑﺎ ﺧﻮاب و ﭘﻮزﻳﺸﻦ ﺑﻴﻤﺎر ،ﻣﺪت درد و ﻧﻴﺎز ﺑﻪ آﻧﺎﻟﮋزﻳﻚ ﻧﻴﺰ ﺑﺮرﺳﻲ ﺷﺪ .اﻧﺴﻴﺪاﻧﺲ ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ در ﺑﻴﻤﺎراﻧﻲﻛﻪ ﺑﺎ ﻟﻴﺪوﻛﺎﻳﻴﻦ اﺳﭙﺎﻳﻨﺎل ﺷﺪه ﺑﻮدﻧﺪ ﺑﻴﺸﺘﺮ ﺑﻮد )%22 P=0/003 (%68 Vs.ﺳﻨﺪرم ﻧﻮروﻟﻮژﻳﻚ ﻣﻮﻗﺖ در %85از ﺑﻴﻤﺎران ﮔﺮوه ﻟﻴﺪوﻛﺎﻳﻴﻦ و %58از ﺑﻴﻤﺎران ﮔﺮوه ﺑﻮﭘﻴﻮاﻛﺎﻳﻴﻦ ﻛﻪ در ﭘﻮزﻳﺸﻦ ﻟﻴﺘﻮﺗﻮﻣﻲ
ﻓﺮﻫﺎد اﻋﺘﻀﺎدي ،ﮔﺮوه ﺑﻴﻬﻮﺷﻲ ،ﺑﻴﻤﺎرﺳﺘﺎن ﺳﻴﻨﺎ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان. آﻳﻼر آﻫﻨﮕﺮي ،داﻧﺸﺠﻮي ﺑﻴﻬﻮﺷﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان، ﺗﻬﺮان ،اﻳﺮان. ﻫﺎﺟﺮ ﺷﻜﺮي ،داﻧﺸﺠﻮي ﺑﻴﻬﻮﺷﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان، ﺗﻬﺮان ،اﻳﺮان. *
ﻧﻮﻳﺴﻨﺪه ﻣﺴﺌﻮل :ﻣﺤﻤﺪرﺿﺎ ﺧﺎﺟﻮي ،ﮔﺮوه ﺑﻴﻬﻮﺷﻲ ،ﺑﻴﻤﺎرﺳﺘﺎن
ﺳﻴﻨﺎ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،ﺗﻬﺮان ،اﻳﺮان.
ﺟﺮاﺣﻲ ﺷﺪه ﺑﻮدﻧﺪ ﺑﺮوز ﻧﻤﻮد .ﺑﻴﻤﺎراﻧﻲﻛﻪ ﻋﻼﻳﻢ داﺷﺘﻨﺪ ﺑﻪﻃﻮر ﻋﻤﺪه
* ﺷﻤﺎره ﺗﻠﻔﻦ0912-3837096 :
در ﮔﺮوه ﻟﻴﺪوﻛﺎﻳﻴﻦ و ﭘﻮزﻳﺸﻦ ﻟﻴﺘﻮﺗﻮﻣﻲ ﺑﻮدﻧﺪ ) .(P=0/002در 77
آدرس :ﺗﻬﺮان ،ﻣﻴﺪان ﺣﺴﻦآﺑﺎد ،ﺧﻴﺎﺑﺎن اﻣﺎمﺧﻤﻴﻨﻲ ،ﻧﺒﺶ ﺳﻲ ﺗﻴﺮ ،ﺑﻴﻤﺎرﺳﺘﺎن ﺳﻴﻨﺎ
E-mail: khajavim@tums.ac.ir
ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ ،داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان ،دوره ،69ﺷﻤﺎره ،7ﻣﻬﺮ 1390
،1390 ،7 ﺷﻤﺎره ،69 دوره ﻏﻼﻣﻌﻠﻲﻲ ﭘﺰﺷﻜ داﻧﺸﮕﺎه ،ﭘﺰﺷﻜﻲ داﻧﺸﻜﺪه و،ﺗﻬﺮان ﺟﻠﻮدار 312 454 ،1390 ﺗﻴﺮ،4ﻣﻬﺮ ﺷﻤﺎره ، 69 ﻫﻤﻜﺎران دوره ،ﺗﻬﺮان ﭘﺰﺷﻜﻲ ﻋﻠﻮمﻋﻠﻮم داﻧﺸﮕﺎه ،ﭘﺰﺷﻜﻲ داﻧﺸﻜﺪه ﻣﺠﻠﻪﻣﺠﻠﻪ
The incidence of transient neurologic syndrome after spinal anesthesia with lidocaine or bupivacaine: The effects of needle type and surgical position: brief report Burning Transient Neurologic Syndrome (TNS) which was first described by Schneider et al in 1993, is defined as a transient pain and dysesthesia in waist, buttocks and the lower limbs after spinal anesthesia.1,2 The incidence of TNS after spinal anesthesia with lidocaine is reported to be as high as 10−40%.3,4 This prospective study was designed to determine the incidence of TNS with two different types of drugs, lidocaine and bupivacaine, in lithotomy or supine positions as the primary outcomes and to determine the association between two different types of needles and surgical positions with the occurrence of TNS as the secondary outcome. The present study was conducted on 250 patients (ASA I-II), aged 18−60 years old, who were candidates for surgery in supine or lithotomy positions. According to the needle type (Sprotte or Quincke) and the local anesthetic (lidocaine or bupivacaine) all patients were randomly divided into four groups. After establishing standard monitoring, spinal anesthesia was performed in all sitting patients by attending anesthesiologists at L2-L3 or L3-L4 levels. The patients were placed in supine or lithotomy position, in regards to the surgical procedure. During the first three postoperative days, patients were observed for post spinal anesthesia complications, especially TNS. Any sensation of pain, dysesthesia, paresthesia or hyperalgesia in the low back area, buttocks, the anterior or posterior thigh, knees, either foot or both feet were recorded. Moreover, duration of pain, its radiation and its relation to sleep and the patients’ position were all carefully considered. Ultimately, the patients’ response to opioid (pethidine) for analgesia was determined. The incidence of TNS was higher when spinal anesthesia was induced with lidocaine (68% vs. 22%, P=0.003). TNS developed in 85% of the patients in lidocaine group and 58% in bupivacaine group after surgery in lithotomy position (P=0.002). In 77 patients pain was in lumbosacral area that radiated to lower limbs and was aggravated in sitting position but in 22 patients pain was in thighs with no radiation. The mean visual analogue scale (VAS) for the determination of pain severity was six in all patients. Pain was alleviated by the administration of pethidine. With regard to the needle type, there were no significant differences between the two types of needles (P=0.7). According to the results of this prospective study, it seems that induction of spinal anesthesia by lidocaine combined with surgical lithotomy position increases the risk of TNS. Our study is in concordance with Keld's study.5 Higher neurotoxicity of lidocaine in comparison with bopivacaine may justify the higher incidence of TNS in the lidocaine group. Moreover, natural lumbar lordosis is maintained better in supine position while it is lost in lithothomy position which may lay traction forces on cauda equina or other nerve roots in the lumbar area leading to neuropraxia. Farhad Etezadi M.D. Department of Anesthesiology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Aylar Ahangary B.Sc. Student of Anesthesiology, Tehran University of Medical Sciences, Tehran, Iran. Hajar Shokri B.Sc. Student of Anesthesiology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Corresponding author: Mohammad Reza Khajavi M.D. Department of Anesthesiology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Address: Hassan Abad Sq., Imam khomini St., Sina Hospital, Tehran, Iran. Tel: +98-912-3837096 E-mail: khajavim@tums.ac.ir
References 1. Schneider M, Ettlin T, Kaufmann M, Schumacher P, Urwyler A, Hampl K, et al. Transient neurologic toxicity after hyperbaric subarachnoid anesthesia with 5% lidocaine. Anesth Analg 1993;76(5):1154-7. 2. Hampl KF, Schneider MC, Ummenhofer W, Drewe J. Transient neurologic symptoms after spinal anesthesia. Anesth Analg 1995;81(6):1148-53. 3. Glaser C, Marhofer P, Zimpfer G, Heinz MT, Sitzwohl C, Kapral S, et al. Levobupivacaine versus racemic bupivacaine for spinal anesthesia. Anesth Analg 2002;94(1):194-8, table of contents.
4. Salazar F, Bogdanovich A, Adalia R, Chabás E, Gomar C. Transient neurologic symptoms after spinal anaesthesia using isobaric 2% mepivacaine and isobaric 2% lidocaine. Acta Anaesthesiol Scand 2001;45(2):240-5. Erratum in: Acta Anaesthesiol Scand 2003;28(3):257. 5. Keld DB, Hein L, Dalgaard M, Krogh L, Rodt SA. The incidence of transient neurologic symptoms (TNS) after spinal anaesthesia in patients undergoing surgery in the supine position. Hyperbaric lidocaine 5% versus hyperbaric bupivacaine 0.5%. Acta Anaesthesiol Scand 2000;44(3):285-90.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره،69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
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14-21 Tehran University Medical Journal; Vol.Journal 64, No. 8, Nov 2006: Tehran University Medical
Tehran UniversityMedical Medical Journal Tehran University Journal Volume 69 Number 7 October 2011 Volume 68 Number 7 October 2010 Volume 64, Number 8, November 2006
Contents The protective effects of Saffron against the oxidative damage in a transient model of focal cerebral ischemia in rats.........................................................................................................................................405 Vakili A, Eianali M.R, Bandegi A.R.
Titrated oral misoprostol solution compared with oxytocin for induction of labor in women with unfavorable cervix....................................................................................................................................413 Niroomanesh Sh, Dadashaliha M, Akrami M.
The comparison between lateral spinal anesthesia and sitting positions in lower limb vascular surgery...420 Mohajer M.R, Karvandian K, Hussain Khan Z, Jafarzadeh A, Dabiran S.
The effects of a single session aerobic exercise on obestatin gene expression in trained women................426 Rashidlamir A, Ebrahimnia M, Hashemi Javaheri A.A.
Total serum magnesium level in icteric neonates before and after phototherapy......................................432 Khosravi N, Aminian A, Taghipour R.
Esophagogastric mesenchymal tumors: analysis of 24 patients.................................................................438 Bagheri R, Maddah Gh, Tavasoli A, Naghavi Riyabi F.
The factors relevant to the onset of vascular complications after coronary intervention in Shahid Rajaei Cardiovascular Center in Tehran, Iran....................................................................................................445 Yousefi A.A, Madani M, Azimi H.R, Farshidi H.
The choanal atresia: 13- year experience and a review of the literature: brief report....................................451 Naraghi M, HajarolAsvadi N.
The incidence of transient neurologic syndrome after spinal anesthesia with lidocaine or bupivacaine: The effects of needle type and surgical position: brief report........................................................................453 Etezadi F, Ahangary A, Shokri H, Khajavi M.R.
1390 ﻣﻬﺮ،7 ﺷﻤﺎره، 69 دوره، داﻧﺸﮕﺎه ﻋﻠﻮم ﭘﺰﺷﻜﻲ ﺗﻬﺮان،ﻣﺠﻠﻪ داﻧﺸﻜﺪه ﭘﺰﺷﻜﻲ
TUMJ
TEHRAN UNIVERSITY MEDICAL JOURNAL The Official Publication of Medical School, Tehran University of Medical Sciences Volume 69
Number 7
October 2011
Chairman: S.H. Emami Razavi Editor in Chief: N. Behtash Executive Editor: M.A. Noyan Ashraf Associate Editors: SH. Akhondzadeh, A. Arab Kheradmand, N. Ataei, S. Borna, M. Ghazi Khansari, S.J. Ghazi Mirsaeed, J. Hajati, M. Kadkhodaei, S. Moradmand, Z. Nadiya Hatmi, M.A. Noyan Ashraf, R. Omranipoor, N. Rezaei, N. Sajjadian Editorial Board: M. Akbarian, F. AmoozegarHashemi, B. Bahar, F. Davari Tanha, N. Ebrahimi Daryani, M.R. Hadiyan, Z. Hallaji, Z. Hussain Khan, M. Kajbaf Zadeh, M.J Mikaeli, A. Mousavi, S.M.J. Mortazavi, B. Nabaei, P. Pasalar , P. Pasbakhsh, M. Rasooli Negad, A. Shaabani, M. Sotoodeh, A.R. Talaeipoor, M. Vahid Dasjerdi, M.R. Zafarghandi International Board: F. Assadi (Chicago), J. Parvizi (Philadelphia), A. Gangi (Strasbourg), M.R. Keshtgar (London), Sh. Masood (Florida), P. Hanjani (Pennsylvania) Editors: N. Behtash, S.B. Hashemi, V. Nikoui, M.A. Noyan Ashraf Office staff: M. Asgari, H. Chaychi, A. Kamizani, R. Ramezani, S. Sadigh Publisher: Tehran University of Medical Sciences Office: Tehran University Medical Journal, Medical School, 202 Amouzesh building, Poursina Ave., Ghods St., Keshavarz Blvd., Tehran, Iran, P.o. Box: 14155-6447, Tel: +98(21)88962510, Fax: +98(21)88962510, Online submission: http://journals.tums.ac.ir/login, and http://tumj.tums.ac.ir, Email: medjournal@tums.ac.ir
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