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 high-performance liquid chromatography (RP-HPLC) 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.
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 high-performance liquid chromatography (RP-HPLC) 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.