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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。
Objective To observe the effect of pinacidil postconditioning on alleviating myocardial ischemia / reperfusion injury in rabbits and to explore its possible mechanism. Methods Forty healthy adult male rabbits were randomly divided into 5 groups (8 in each group): sham group, I / R group, I-postC group, , Pinacidil after treatment group (Pina), pinacidil after treatment + 5-hydroxy acid group (Pina + 5-HD). The models of myocardial ischemia / reperfusion injury were duplicated by ligating left anterior descending coronary artery for 30 min / reperfusion for 120 min. The cardiac function, plasma CK activity and MDA content were observed and compared before ischemia, 30 min ischemia and 120 min reperfusion. Myocardial ischemia and infarct size, expression of Bcl-2 and Bax mR-NA were measured. Results Compared with I / R group and Pina + 5-HD group, LVSP in I-postC group and Pina group increased significantly (P <0.05) and LVEDP decreased significantly (P <0.05) at 120 min after reperfusion. (P <0.05); the area of myocardial infarction was significantly decreased (P <0.05); the expression of Bcl-2 mRNA was significantly increased and the expression of Bax mRNA was significantly decreased (P <0.05) <0.05). Conclusion Pinacidil postconditioning can relieve myocardial ischemia / reperfusion injury by simulating myocardial protection mechanism after ischemic postconditioning. The mechanism of myocardial protection may involve the opening of mitochondrial ATP-sensitive potassium channels, the up-regulation of Bcl-2 mRNA expression and Down-regulation of Bax mRNA expression.