[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 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.


CONCLUSIONS
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.
Chen
Jian-bin
JB
Department of Internal Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Rao
Bang-fu
BF
Chang
Jing
J
Liao
Xiao-gang
XG
Cao
You-de
YD
D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D002216:Captopril / Q000494:pharmacology*; D003384:Coxsackievirus Infections / Q000188:drug therapy* / Q000503:physiopathology; D004734:Energy Metabolism; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008928:Mitochondria / Q000378:metabolism; D009205:Myocarditis / Q000188:drug therapy* / Q000503:physiopathology / Q000821:virology; D009206:Myocardium / Q000378:metabolism; D011897:Random Allocation; D013385:Succinate Dehydrogenase / Q000378:metabolism
D000806:Angiotensin-Converting Enzyme Inhibitors; D002216:Captopril; D013385:Succinate Dehydrogenase