维药爱维心对离体大鼠心肌缺血/再灌损伤作用机制研究

目的探讨维药爱维心在缺血/再灌(I/R)损伤过程中对大鼠离体心脏心功能、心律失常、心肌细胞活性、心肌酶及心肌细胞凋亡的保护作用及其可能的作用机制。方法采用离体大鼠心脏Langendorff灌流模型,全心停灌30min,再灌60min建立I/R模型。用MedLab生物信号采集处理系统记录分析血流动力学及心律失常指标;实验结束检测心肌组织中甲臜(formazan)含量;测定再灌注各时间点心脏流出液中乳酸脱氢酶(lactate dehy-drogenase,LDH)的含量;SABC免疫组织化学法检测心肌细胞凋亡指数;透射电子显微镜观察心肌超微结构的改变。结果与对照组比较,爱维心5mL/L处理组能够明显降低缺血/再灌引起的大鼠离体灌流心脏左心室舒张末期压力(LVEDP),增强左心室最大舒张速率(-dp/dtmax)和心脏做功(rate-pressure product,LVDP×heartrate,RPP)(P<0.01),降低I/R心肌LDH含量(P<0.01),下调凋亡指数(P<0.01),并且能降低缺血心肌细胞的线粒体损伤程度。结论爱维心可改善离体大鼠I/R损伤心肌顺应性,保护和稳定心肌细胞膜,并有抑制心肌细胞凋亡的作用。

Effect of Aiweixin on isolated rat heart during ischemia/reperfusion injury

Objective To investigate the effect of Aiweixin on the heart function,arrhythmia,activity of cardiac myocyte,creatase content and myocardial apoptosis of isolated rat heart during ischemia/reperfusion injury.Methods The isolated perfused rat hearts on langendorff apparatus were subjected to global ischemia for 30 min and followed by 60 min of reperfusion.Hemodynamic and arrhythmia index were determined by MedLab bioinformation collection and treatment system.Lactate dehydrogenase(LDH) and Myocardial viability were measured by spectrophotometrically assay.Myocardial ultrastructure was observed by transmissionelectron microscopy;Apoptosis of cardiocyte was determined of by SABC immunohistochemistry.Results Compared with control group,Aiweixin(5 mL/L) significantly attenuated the inhibitory effects induced by ischemia on LVEDP,-dp/dtmax and rate-pressure product(RPP,P<0.01);decreased the content of LDH in the ischemia myocardium(P<0.01);obviously down regulated the apoptosis index(P<0.01),and decreased the mitochondrion injury degree in ischemia cardiocyte.Conclusion Aiweixin can improve the compliance of the myocardium during ischemia/reperfusion injury,promote the stability of cell membrane;inhibited the apoptosis of cadiocyte.