Objective： To explore the pathophysiological changes of chronic heart failure resulting from pressure overload in juvenile and the effects of carvedilol. Methods： The animal model of CHF was established by constriction of abdominal aorta. Four weeks after operation， the rats were randomly divided into 3 groups： sham-operated group， CHF group， carvedilol group. Carvedilol was administered by direct gastric gavage. Eight weeks after operation， the hemodynamic analysis， the pathologic analysis of hearts and the cardiac myocyte apoptosis analysis were performed. The serum contents of lipid pereoxidation（LPO） and superoxide dismutase（SOD） were detected. Results： Compared with the sham-operated group， SBP， DBP， LVSP， LVEDP， LVRW， RVRW， LPO， AI were all significantly increased（P < 0.01） in CHF group. A significant decrease could be seen in +dp／dtmax， -dp／dtmax， SOD in CHF group. A significant decrease could be seen in SBP， DBP， LVSP， LVEDP， LVRW， RVRW， LPO， AI in carvedilol group compared with CHF group. While a significant increase could be seen in +dp／dtmax， -dp／dtmax and SOD（P < 0.01）. Conclusion：The ventricular remodeling， the myocardial apoptosis and oxidative stress may take part in the pathogenesis and progression of CHF， which might be inhibited by carvedilol.