Objective:To explore the improving effect of Salvianolic acid A (Sal A) on pressure overload-induced cardiac dysfunction and ventricular remodeling in rats. Methods:The pressure overload rat model was established by transverse aortic constriction(TAC). The Sal A was applied at the concentration of 5 mg/(kg-d) by gavage for continuous 12 weeks,and some rats with pressure overload were treated with the same volume of saline. The rats were assigned into 4 groups:Sham-saline,TAC-saline,Sham-Sal A and TAC-Sal A. Twelve weeks later,hemodynamic conditions,heart function and heart anatomy indicators were analyzed among 4 groups. Hematoxylin-eosin (HE),Masson＇s triple staining and specific fluorescent probe DHE were performed to analyze the morphology,fibrosis and reactive oxygen species levels of myocardial cell. The protein levels of apoptosis related genes were evaluated by Western blotting. Results:Compared with the Sham-saline group,TAC operation led to a decrease of heart rate,mean left ventricular systolic pressure,left ventricular pressure maximal rate and protein level of Bcl-2 (anti-apoptosis gene),and an increase of left ventricular end-diastolic pressure,cardiac diameter,collagen volume fraction,heart weight ratio,myocardial fluorescence intensity and protein levels of Bax and Cleave caspase-3 (pro-apoptotic gene). After the treatment with Sal A,the above indicators got attenuated. However,there were still significant differences on mean systolic pressure of left ventricular,heart weight ratio,cardiac diameter,collagen volume fraction and protein levels of apoptosis-related genes between the group of Sham-saline and the group of TAC-Sal A(P < 0.05). The treatment with Sal A had no effect on the indicators of Sham rats. Conclusion:Sal A can improve pressure overload-induced cardiac dysfunction and attenuate and protect ventricular remodeling including myocardial hypertrophy,fibrosis and apoptosis.