缺血后处理对减轻兔心肌缺血再灌注损伤作用的研究

目的观察缺血后处理在减轻家兔心肌缺血再灌注损伤中的作用,并探讨其可能机制。方法将32只健康成年雄性家兔随机分为4组(每组8只),分别为假手术组(Sham)、缺血再灌组(I/R)、缺血后处理组(I-postC)、缺血后处理+5-羟葵酸组(I-postC+5-HD)。采用结扎左冠前降支30 min/复灌60 min的方法复制心肌缺血再灌注损伤模型。观察并比较各组动物在缺血前、缺血30 min、复灌60 min时LVSP和LVEDP值、血浆CK活性和MDA含量,测定心肌缺血和梗死面积。结果在复灌60 min时,与I/R组相比,I-postC组LVSP明显升高(P<0.05);LVEDP明显降低(P<0.05);血浆CK活性明显降低(P<0.05);血浆MDA含量明显降低(P<0.05);心肌梗死面积明显减小(P<0.05)。比较I/R组和I-postC+5-HD组LVSP、LVEDP、血浆CK活性和MDA含量未见明显差异,梗死面积也未见差异。结论缺血后处理可通过开放线粒体ATP敏感性钾通道,减轻心肌缺血再灌注损伤。

Effect of Ischemic Postconditioning on Alleviating Myocardial Ischemia-Reperfusion Injury in Rabbits

Objective To investigate the effects of ischemic postconditioning on alleviating myocardial reperfusion injury in rabbit in vivo and explore its potential mechanisms.Methods Thirty-two healthy and adult male rabbits were randomly divided into four groups(n=8 in each group): Group 1(Sham),Group 2(ischemic reperfusion),Group 3(ischemic postconditioning) and Group 4(ischemic postconditioning and 5-HD).The model of ischemic reperfusion injury was made by occluding the left anterior descending artery for 30 min and reperfusion for 60 min in rabbit heart.The index of LVSP,LVEDP,plasma creatine kinase activity and malondialdehyde content were measured and compared at baseline,the end of ischemia and after 60 min of reperfusion respectively.Myocardial ischemic and infarct size was determined at the end of the experiment.Results At 60 min of reperfusion,compared with Group 2,LVSP was significantly higher in Group 3(P<0.05);LVEDP,plasma CK activity,Plasma MDA content and myocardial infarct size were significantly reduced(P<0.05).There were no differences in LVSP,LVEDP,CK activity,MDA content and infarct size between Group 2 and Group 4.Conclusion Ischemic postconditioning can alleviate the reperfusion injury via opening mitochondrial ATP-sensitive potassium channels.