Effect of carvedilol on mitochondrial respiratory function of pressure overload induced left ventricular hypertrophy in rats and its mechanism
- VernacularTitle:卡维地洛对压力超负荷大鼠肥厚心肌线粒体呼吸功能的影响及其机制
- Author:
Rong SONG
;
Jiang WANG
;
Ling NIE
;
Shanjun ZHU
- Publication Type:Journal Article
- Keywords:
Ventricular remodeling;
Mitochondria;
Beta-adrenergic receptor antagonist
- From:
Journal of Medical Postgraduates
2004;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To understand the effect of Carvedilol on mitochondrial oxidative phosphorylation function during the development of pressure overload induced left ventricular hypertrophy in rats and its mechanism.Methods: Male SD rats were randomized into 6 groups: 5-and 15-week coarctation of the abdominal aorta(H5,H15),5-and 15-week Carvedilol intervention(HR5,HR15) and 5-and 15-week sham operation(S5,S15).Hemodynamics and ventricular remodeling parameters were measured,and the mitochondrial respiratory function was detected by Clark oxygen electrode.Results: Compared with S5,mitochondrial state 3 and 4 respiration and the oxidative phosphorylation rate(OPR) were increased and the respiratory control rate(RCR) decreased significantly in the H5 group.In comparison with S15,state 3 respiration,OPR and RCR were reduced significantly in the H15group.Carvedilol increased the three parameters and restored them to the level of the S15.Conclusion: Mitochondrial respiratory function decreased during the development of pressure overload induced left ventricular hypertrophy in rats.Carvedilol could protect mitochondrial respiratory function and improve myocardial energy metabolism,which might be a mechanism underlying its protective effect on myocardium.