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作 者:蒋华[1] 虞燕琴[1] 蒋峻[1] 张蓓[1] 沈岳良[1] 夏强[1]
出 处:《浙江大学学报(医学版)》1999年第6期241-244,共4页Journal of Zhejiang University(Medical Sciences)
基 金:卫生部;浙江省自然科学基金;浙江省卫生厅科研基金
摘 要:目的:研究KATP通道在离体大鼠心脏缺血预处理中的作用。方法:取雄性SD大鼠心脏行Langendorff灌流。以3m in 全心缺血加5m in 复灌重复3次为预处理,灌流30 m in 作为对照,同时灌以KATP通道阻断剂优降糖(10 μm ol/L)或开放剂吡那地尔(50 μm ol/L)。然后以结扎左冠状动脉20 m in,复灌60 m in 作为缺血复灌,以心肌梗塞范围和心律失常评分作为指标,观察药物对预处理的心肌保护作用的影响。结果:优降糖可阻断缺血预处理的作用,而吡那地尔则不能模拟缺血预处理,但是在缺血期间吡那地尔对心肌有保护作用。结论:KATP通道很可能参与了大鼠心肌缺血预处理的心肌保护机制。Objective:To study the role of ATP sensitive potassium channels in ischemic preconditioning of isolated rat hearts.Methods:Hearts were isolated from male SD rats,and perfused on a Langendorff apparatus.Rat hearts were pretreated with 3 min global ischemia followed by 5 min reperfusion for three times or as ischemic preconditioning and perfused for 30 min as control.The K ATP channel blocker——glibenclamide (10 μmol/L) or opener——pinacidil (50 μmol/L) was preperfused in this stage.Then the left coronary artery was occluded for 20 min and reperfused for 60 min to observe the effects of drugs on myocardial infarct size and arrhythmic scores.Results:The action of ischemic preconditioning was blockaded by glibenclamide,and pinacidil failed to mimic the ischemic preconditioning.But pinacidil treatment just before ischemia was cardioprotective.Conclusions:It seems that K ATP channels take part in the promotion of ischemic preconditioning and the cardioprotective mechanisms in rat hearts,although they are not the trigger.
关 键 词:钾通道 ATP敏感性钾通道/生理学 缺血预处理 心肌 大鼠
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