The influence of oxygen stress on cardiac apoptosis in heart failure rats and the interference of carvedilol

Objective:To investigate the influence of oxygen stress on the level of cardiac apoptosis index(AI) in chronic congestive heart failure rats,and to intervene with the third-generation blocker-carvedilol to elucidate its mechanism.Methods:8 weeks after partially banding abdominal aortic artery,20 Wister rats were randomly assigned into two groups:①heart failure group( n =10);②carvedilol group( n =10).Meanwhile,sham-operated rats( n =10) were established as a control group.After 4 weeks of remedy,hemodynamic parameters,ventricular mass index(LVMI and RVMI),oxygen stress including superoxide dismutase (SOD) and malondialdehyde (MDA),and myocardiac apoptosis were studied.Results:①Compared with sham-operated rats,all the hemodynamics were deteriorated,and LVMI and RVMI were increased significantly ( P 0.01～0.05).Plasma MDA was on rise while SOD decreased ( P 0.01),and cardiac apoptosis index was risen to 48.89% in heart failure rats ( P 0.001).②LVMI was positively related to the index of apoptosis, r =0.767 ( P 0.01).In addition,myocardial apoptosis level was positively associated with plasma MDA but negatively with SOD activity, r =0.701,-0.636( P 0.05),respectively.Apoptosis was paralleled with worsening heart function ( P 0.001～0.05).③After carvedilol therapy,LVMI and RVMI decreased and SOD and MDA improved( P 0.01～0.05).Heart function was also ameliorated,including systolic and diastolic function( P 0.01～0.05).Moreover,cardiac apoptosis decreased significantly( P 0.01).Conclusion:Oxygen stress may be critical for activation of cardiac apoptosis in the over-loaded heart.Apoptosis involves in ventricular remodeling,predicting the prognosis of heart failure.Carvedilol can ameliorate heart function,whose mechanism may be in its improvement of oxygen stress,and inhibition of cardiac apoptosis and reversion of ventricular remodeling.