Résumé
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.