【摘要】 目的 探讨缺血后适应(IPost)在离体小鼠肥厚心肌缺血再灌注(I/R)损伤中的保护作用及可能的作用机制。方法 12周龄C57/BL小鼠通过主动脉弓缩窄4周建立心肌肥厚模型,利用Langendorff灌流装置建立小鼠肥厚心肌I/R模型,稳定灌流10 min后分为3组,空白组(SH组,给予灌流液持续灌流150 min)、缺血再灌注组(I/R组,予30 min全心缺血随后再灌注120 min)、缺血后适应组(IPost组,予30 min全心缺血后,采取缺血10 s及再灌注10 s的3次IPost周期,再灌注120 min)。使用微球囊进行心脏血流动力学检测,采用三苯基氯化四氮唑染色的方法确定梗死心肌面积及生化法测定心肌酶、检测心肌细胞超微结构,TUNEL法检测心肌细胞的凋亡。结果与SH组I、/R组比较,IPost组小鼠心脏血流动力学指标LVSP、dp/dtmax显著改善,心肌梗死范围减小,心肌酶释放减少,调亡指数显著降低(P均<0.05)。与I/R组比较,IPost组透视电镜下心肌细胞线粒体损伤明显减轻。结论 IPost能通过减少心肌梗死范围、减少线粒体损伤、抗心肌凋亡而有效地减轻离体小鼠肥厚心肌缺血再灌注损伤。更多还原

【Abstract】 Objective To determine the effect of ischemic postconditioning（IPost） protection in hypertrophic myocardium subjected to ischemic-reperfusion（I/R） injure and its possible mechanism.Methods Transversing aortic constriction（TAC） was induced in aged 12 wks old C57/BL mice to establish left ventricular hypertrophy for 4 wks.Hypertrophic myocardium I/R injure was induced by 30 min globe ischemia,followed by 120 min reperfusion in Langendorff model.Hearts were randomly divided into 3 groups: sham group;I/R group;IPos group(three cycles of 10s reperfusion interspersed by 10s of no-flow ischemia.At the end of hemodynamic determination,infarction size（IS） measurement were performed,assess ultrastructural organizationin myocardium.Apoptosis was measured by TUNEL staining.Results Compared with sham group and I/R group,IPost group had higher Lvsp,dp/dt_max;Infarct sizes and apoptotoc index were significantly reduced;Meanwhile,Mitochondria injury of cardiac myocyte at electron microscope was obviously lightened.Conclusion IPost has protective effect in hypertrophic myocardium with I/R injure in vitro by reduced infarction size,lightened mitochondria injury and opposed apoptosis.更多还原