阿托伐他汀和尼可地尔后处理对兔心肌缺血再灌注心功能及Bcl-2、Bax的影响

The Effect of Atorvastatin and Nicorandil on Bcl-2and Bax in Isolated and Reperfusion Rabbit Hearts

目的:建立缺血再灌注模型,观察阿托伐他汀和尼可地尔后处理对兔心肌缺血再灌注心功能及Bcl-2、Bax的影响。方法:50只大白兔随机分成5组[假手术组(A)、对照组(B)、阿托伐他汀组(C)、尼可地尔组(D)、联合后处理组(E)],采用"二线二结法"建立缺血再灌注模型。各组按照实验设计方案给药,记录心电图、血流动力学指标。采集血液标本,试剂盒检测CK、cTnI。电镜下观察各组心肌细胞超微结构变化。双色实时荧光定量PCR检测Bcl-2、Bax。结果:(1)再灌注2h,C^E组LVSP高于B组(P<0.05),±dp/dt max高于B组(P<0.01),而LVEDP低于B组(P<0.01)。其中,C、D组无显著性差异,E组LVSP、±dp/dt max均高于C、D组(P<0.05),LVEDP显著低于C、D组(P<0.05)。(2)再灌注2h,B^E组CK与A组比较均明显升高(P<0.01),B组最高(P<0.01),D组高于E组(P<0.01);再灌注2h,B^E组cTnI较缺血前明显升高(P<0.05);C^E组显著低于B组(P<0.01),E组与C、D组比较有显著差异(P<0.05)。(3)电镜显示C^E组心肌细胞的损伤明显减轻。(4)B^E组BCL-2mRNA表达较A组增高(P<0.05),其中C^E组BCL-2 mRNA表达又较B组增高(P<0.01);B^E组Bax mRNA表达较A组增高(P<0.05),其中C^E组Bax mRNA表达又较B组减少(P<0.01)。结论:阿托伐他汀、尼可地尔后处理对兔心肌缺血再灌注损伤有保护作用,可能通过影响BCL-2、Bax mRNA表达抑制心肌细胞的凋亡,对缺血再灌注心肌产生保护作用。

Objective：To observe the heart function and Bcl-2,Bax of Atorvastat in and Nicorandil on ischemia and reperfusion induced injury in rabbit heart.Methods：50rabbits were randomly divided into 5groups,and the myocardial ischemiareperfusion were generated by two sutures and two knots,then administrated in accordance with the experimental design,monitoring ECG and left ventricular pressure,testing CK,cTnI in serum,observing the changes of myocardial structure,testing Bcl-2and Bax by RT-PCR.Results：The LVSP and±dp/dt max levels of group C-E were significantly higher than that of group B（P〈0.05）.On the contrary,the LVEDP was lower than that of group B（P〈0.01）.The CK and cTnI levels of group C-E were lower than B（P〈0.01）.The injury of group B was worse than C-E of the cellular structure under EM.The BCL-2and Bax mRNA levels of group B-E were significantly higher than that of group A（P〈0.05）,and BCL-2C-E higher than B,The contrary,however,the bax was lower than that of group B.Conclusion：Myocardial isehemic postconditioning of Atorvastatin and Nicorandil induced cardio protection on ischemia reperfusion injury in rabbits.They can improve myocardial systolic and diastolic function,maybe through reducing cell apoptosis.