目的:探讨远距缺血后处理对大鼠急性心肌缺血/再灌注损伤的影响及其可能存在的机制。方法:将24只雄性SD大鼠随机均分为缺血/再灌注组和远距缺血后处理组。实验过程中监测心电图Ⅱ导联指标,再灌注结束后分别测定血浆乳酸脱氢酶(LDH)、肌酸激酶(CK)活性以及心肌梗死面积。应用RT-PCR技术检测心肌组织中Bax和Bcl-2 mRNA基因表达情况。结果:与缺血/再灌注组相比,远距缺血后处理组大鼠心律失常发生评分明显降低(P〈0.01),LDH及CK活性降低(P〈0.01),心肌梗死面积百分比减小(P〈0.05),大鼠心肌组织中Bcl-2/Bax比值升高(P〈0.05)。结论:远距缺血后处理对心肌缺血/再灌注损伤具有明显的保护作用,其机制可能与抗细胞凋亡有关。
Objective:To investigate the mechanism of remote ischemic postconditioning(RPostC) induced cardioprotection against ischemia/reperfusion(I/R) injury in rat model.Methods:Anesthetized male Sprague Dawley rats were randomly divided into the two groups,ischemia/reperfusion(I/R,n=12) and remote ischemic postconditioning group(RPostC,n=12).Throughout the experiment,a lead Ⅱ electrocardiogram was continuously monitored.At the end of reperfusion,arterial blood sample was obtained to quantify plasma activity of lactate dehydrogenase(LDH) and creatine kinase(CK).The infarct size was measured by triphenyltetrazolium chloride staining method.The expressions of Bcl-2 and Bax at mRNA level of left anterior myocardium were detected by RT-PCR analysis.Results:Compared with the I/R group,the levels of ventricular arrhythmia,CK,LDH release and infarct size in RPostC group were reduced significantly(P0.01 and P0.05);and the ratio of Bcl-2/Bax mRNA expression was increased(P0.05).Conclusions:Remote ischemic postconditioning has the significant protective effect on rat against myocardial ischemia and reperfusion injury,and the anti-apoptosis might be a mechanisms of cardioprotection.