骨骼肌缺血预适应对心脏的保护作用

Study on myocardial protection provided by skeletal muscle ischemic preconditioning

目的:确定骨骼肌缺血预适应对心肌坏死面积、超微结构及冠状动脉内皮相关因子的影响。方法:12只小型猪被随机分成缺血对照(C)组和远端预适应(RP)组,采用非开胸法建立心脏缺血再灌注(I/R)模型,通过球囊闭塞左股动脉造成骨骼肌短暂缺血。以三硝基四氮唑红确定心肌梗死范围;以电镜观察缺血心肌超微结构;同时动态观察I/R过程中左前降支(LAD)冠状动脉血中NO、血管性假血友病因子(vWF:Ag)、内皮素-1(ET-1)及丙二醛含量变化。结果:与C组相比,RP组明显减少心肌梗死范围,减轻心肌超微结构损伤,并明显增加LAD冠状动脉内的NO含量、降低vWF:Ag和ET-1的含量。结论:骨骼肌RP减少I/R所致心肌梗死范围,保护心肌超微结构,并对损伤冠状动脉内皮有一定保护作用。

Objective： To determine the effect of skeletal muscle ischemic preconditioning on myocardial infarct area, ultrastructure of ischemic myocardium and plasma concentrations of nitric oxide （NO）, von Willebrad （vWF：Ag）, ET-1 in coronary artery during ischemia reperfusion （I/R）. Method： Twelve pigs were randomized into control （C） group and remote preconditioning （RP） group. The myocardial infarct size was examined with triphenyl tetrazolium choride （TTC）, and ultrastructure of ischemic myocardium was observed by electron microscope. Blood samples were taken from left anterior descending artery （LAD） at different time points for assessing the concentrations of NO, vWF Ag, ET landMDA. Result： ①In group C, the myocardial infarct size, expressed as a percent of the ischemic myocardium was（51. 1±2.3）%, and it was reduced to （24. 1±1.5）% in group RP （ P 〈0.05）. ②Electron microscopic myocardial damage in group RP was less severe than that in group C. ③ There was a decrease of NO concentration at the beginning of reperfusion in group C, but it was increased significantly at the same time in group RP. On the other hand, concentrations of vWF：Agand ET-1 were increased during reperfusion in group C, but they were lower in group RP than those in group C. The amount of MDA was increased at the end of reperfusion, and was much higher in group C than that in group RP. Conclusion： RP induced by skeletal muscle ischemia could not only reduce myocardial infarct size and protect ultrastructure, but also pro tect coronary endothelial function from injury by I/R, which might be mediated by oxidative radicals.