卡托普利对病毒性心肌炎小鼠心肌能量代谢的保护作用

目的：探讨病毒性心肌炎(VMC)小鼠心肌能量产生状况，并用卡托普利进行干预治疗。方法：雄性Palb／c小鼠随机分为柯萨奇B3病毒(CVB3)感染组、CVB3感染加卡托普利治疗组和对照组。分别采用电镜和形态计量学方法观察心肌线粒体形态、数量和膜磷脂定位；酶细胞化学法分析线粒体细胞色素氧化酶(CCO)和琥珀酸脱氢酶(SDH)活性，反相高效液相色谱法测定心肌组织ATP、ADP和AMP含量。结果：感染组小鼠心肌线粒体大量破坏，膜磷脂严重缺失、定位改变，CCO和SDH活性降低，ATP、ADP和AMP含量下降。不同时间点治疗组上述各项指标均较感染组显著改善。结论：VMC心肌线粒体结构严重破坏、功能明显下降，卡托普利能有效保护VMC心肌线粒体结构和功能，改善心肌能量代谢。

Effects of captopril on myocardial energy metabolism in mice with viral myocarditis

Objective: To explore the changes of myocardial energy production in mice with viral myocarditis,and to observe the interventional effects of captopril. Methods: The male Balb/c mice were randomly divided into three groups: coxsackie B3 virus(CVB3) infection group (infection group), CVB3 infection group with captopril treatment(treatment group) and control group. The morphology, membrane phospholipid, as well as activities of cytochrome oxidase(CCO) and succinate dehydrogenase(SDH) of myocardial mitochondria were studied by using transmission electron microscope, morphometry and enzyme cytochemical method respectively . Reversed phase highperformance liquid chromatography(RPHPLC) was used to analyze contents of myocardial ATP, ADP and AMP. Results: A large number of mitochondria were damaged in infection group, the apparent mitochondrial membrane phospholipid deletion and localization change were observed , the activities of CCO and SDH in mitochondria declined obviously, and the contents of ATP, ADP as well as AMP declined notably. All of these were improved significantly in treatment group . Conclusion : The myocardial mitochondrial structure destroys and its functions decline apparently in viral myocarditis. Captopril has effects against myocardial mitochondrial structure damage and function decline, ameliorate myocardial energy metabolism.