Objective:To study the effect and possible mechanism of Poge Jiuxin decoction(PGJXD) on heart failure(HF) after infarction induced by Yang weak and body fluid flood syndrome in rats. Method: Rat model of HF was induced by adriamycin. The model-established rats were randomized into model group

PGJXD high-dosage group(18.66 g·kg-1)

low-dosage group(9.33 g·kg-1) and the fosinopril sodium group(4.67 mg·kg-1). A blank control group was also set up. Drugs were given by continuous intragastric administration for 28 days. Then cardiac function of each group was evaluated by echocardiography

plasma aldosterone(ALD) and angiotensin Ⅱ(AngⅡ) levels were also examined by radioimmunoassay(RIA) in all groups

and myocardial pathology biopsy was carried out. Result: Compared with the blank group

the left ventricular end-diastolic diameter(LVEDd) and left ventricular end-systolic diameter(LVEDs) of model group increased significantly(P<0.05)

ejection fraction(EF)decreased significantly(P<0.05). After given the high-dose and middle-dose of PGJXD and the fosinopril sodium

EF and cardiac function were improved. Moreover

PGJXD could effectively shorten the LVEDd and LVEDs

and fosinopril sodium did not work. RIA results showed that ALD and AngⅡ in plasma of model group was significantly higher than those in blank group(P<0.05);the high-dose and middle-dose of PGJXD and the fosinopril sodium could down-regulate the plasma ALD and AngⅡ(P<0.05). In the models

myocardial pathology investigation suggested myocardial fibers derangement

with visible dyeing depth

fracture and zoning

part of the muscle fibers were separated from each other. Compared with the model group

the high-dose and middle-dose of PGJXD and the fosinopril sodium showed obvious reduced myocardial fiber breakage. Conclusion: PGJXD can shorten the LVEDd and LVEDs

and thus reverse myocardial remodeling and strength the cardiac function. The mechanism may be related to decrease in plasma ALD and AngⅡ and reduce in renin-angiotensinrenin-angiotensinaldosterone system(RAAS) activity thus to improve cardiac afterload in HF Rats.