预处理对心肌缺血-再灌注损伤保护作用及其部分保护机制的探讨

The protective role of ischemic preconditioning in ischemia/reperfusion and its partly protective mechanism

目的:用结扎冠状动脉制造心肌梗塞模型的方法观察预处理对大鼠心肌坏死范围和细胞凋亡及其调控基因bcl-2等的影响。mRNA方法:在缺血再灌注,结扎冠状动脉前注射给心肌次、每次缺血间隔再灌注90min/180min5min35min5min为心肌缺血预处理组();结扎股动脉松开再结扎冠状动脉为结扎股动脉组();结扎肠系膜动脉IPC15min10minFAO15松开再结扎冠状动脉为结扎肠系膜动脉组();结扎冠状动脉前不做任何干预的为对照组()。min10minMAOI/R.结果:3组预处理组测得的心肌坏死范围()分别为%23.5±、1.524.3±、1.723.8±、1.224.2±、4.117.6±与组1.7I/R35.9±相比2.1P<;经测得的为0.01RT-PCRbcl-2mRNA0.900±、0.040.891±、0.040.875±与0.02I/R.0.817±相比。0.02结论:()预处1理对心肌坏死范围有保护作用;()预处理保护心肌的部分机制是通过上调细胞凋亡基因,减少心肌梗塞区域2Bcl-2mRNA细胞凋亡数量等而实现的。

Objective: We observed the changes of myocardiocytes apoptosis and the expression of bcl-2mRNA after the intervention by myocardial ischemic preconditioning(IPC), brief occlusion of anterior mesenteric artery (MAO) and femoral artery(FAO), in order to obtain the partial cardial myoctes protective mechanism of them. Methods: 56 Wistar rats divided into I/R., IPC, FAO, and MAO groups were tested, using in situ TdT-mediated dUTP nick end labeling(TUNEL), and RT-PCR methods. Results: We obtained these ischemic preconditionings which reduced the rats` infarction size(35.9%±2.1%vs17.6%±1.7%, 24.3%±1.7%, 23.5±1.7%) by reducing the myocardiocyts apoptosis(24.67%±4.18vs9.56%±2.43%, 13%±4.29%, 15%±5.09%) through the upregulation of bcl-2 mRNA(0.82±0.02VS0.91±0.04, 0.89±0.04, 0.88±0.02). Conclusion: The trial results can be summarized as follows: IPC, FAO, and MAO can reduce the rats' ventricular myocardial infarction size; the partial myocardial protective mechanisms of IPC, FAO, and MAO can be obtained by the upregulation of bcl-2 mRNA. The preventive effect of bax mRNA by these interventions is under research.