吡那地尔后处理在减轻家兔心肌缺血/再灌注损伤中的作用

目的观察吡那地尔后处理在减轻家兔在体心肌缺血/再灌注损伤的作用,并探讨其可能机制。方法 40只健康成年♂家兔随机分为5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)、吡那地尔后处理组(Pina)、吡那地尔后处理+5-羟葵酸组(Pina+5-HD)。采用结扎左冠前降支30 min/复灌120 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120 min时心功能指标、血浆CK活性和MDA含量。测定心肌缺血和梗死面积,Bcl-2和Bax mR-NA的表达。结果在复灌120 min时,与I/R组和Pina+5-HD组相比,I-postC组和Pina组动物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);Bcl-2 mRNA的表达明显增加,BaxmRNA的表达明显降低(P<0.05)。结论吡那地尔后处理可通过模拟缺血后处理的心肌保护机制,减轻心肌缺血/再灌注损伤,其心肌保护的机制可能涉及线粒体ATP敏感性钾通道开放,Bcl-2 mRNA表达的上调和Bax mRNA表达的下调。

Effects of Pinacidil postconditioning on relief of myocardial reperfusion injury

Aim This study aimed to investigate effects of Pinacidil postconditioning on the relief of myocardial reperfusion injury in rabbit in vivo and explore its possible mechanisms.Methods Forty healthy adult male rabbits were randomly divided into five groups(n=8 in each group):Group1(Sham),Group2(ischemic reperfusion),Group3(ischemic postconditioning),Group 4(Pinacidil postconditioning),Group5(Pinacidil and 5-HD postconditioning).The model of ischemic reperfusion injury was made by occluding the left anterior descending artery for 30 min and reperfusing for 120 min in rabbit heart.The index of cardiac function,plasma creatine kinase activity and malondialdehyde content were measured and compared at baseline,the end of ischemia,and after 120 min of reperfusion respectively.Myocardial ischemic,infarct size,expression of Bcl-2 and Bax mRNA in myocardium were determined at the end of the experiment.Result At 120 min of reperfusion,compared with Group 2 and Group 5,LVSP was significantly higher in Group 3 and 4(P<0.05);LVEDP,plasma CK activity,and Plasma MDA content were significantly lower(P<0.05);myocardial infarct size was significantly reduced in Group 3 and 4(P<0.05);expression of Bcl-2 mRNA increased remarkably;Bax decreased remarkably(P<0.05).Conclusion Pinacidil postconditioning provides potent reduction of reperfusion injury,which is similar to the cardioprotective effect of ischemic postconditioning.The potential mechanisms of this phenomenon might be associated with mitochondrial ATP-sensitive potassium channel opening,increased expression of Bcl-2 mRNA and decreased Bax mRNA.