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.