Aim To observe the effects of alprostadil on the expressions of metalloproteinase-2 （MMP-2） and metalloproteinase-9 （MMP-9） and fibrosis in myocardial tissues of rats with chronic heart failure. Methods Seventy male SD rats were randomly divided into sham operation group and model group. Rats in model group were made by abdominal aorta coarctation. Four weeks later,the model rats were randomly divided into four groups according to different concentrations of alprostadil: untreated group,low dose group,medium dose group and high dose group. After two weeks,myocardial collagen fibers were evaluated through Masson staining and collagen volume fraction （CVF） was measured. The contents of hydroxyproline （HYP） and the total collagen in myocardium were tested. The mRNA expressions of MMP-2 and MMP-9 in myocardial tissues were detected by real-time fluorescence quantitative polymerase chain reaction and activities of MMP were assayed by zemography. Results Compared with untreated group,CVF,HYP and the total collagen contents in myocardial tissues of rats were decreased significantly （P<0.05 or P<0.01） in all drug-treated groups. The mRNA expression levels and activites of MMP-2 and MMP-9 were significantly lower in drug-treated groups than in untreated group （P<0.05 or P<0.01）. There was no statistically signicant difference of the mRNA expression between low dose group and medium dose group （P>0.05）. The mRNA contents of MMP-2 and MMP-9 were decreased significantly in high dose group compared with low dose group and medium dose group （P<0.05）. The levels of MMP-2 and MMP-9 activates were significantly decreased with the concentration of alprostadil （P<0.05 or P<0.01）. Concentrations of alprostadil are inversely correlated with CVF,HYP,total collagen contents,mRNA expressions and activates of MMP-2 and MMP-9 in myocardial tissues of rats （P<0.05 or P<0.01）. Conclusions Alprostadil can decrease the expressions and activition of MMP-2 and MMP-9 in myocardial tissue of rats with chronic heart failure,which may be the important mechanism in delaying the myocardial fibrosis progression,preventing cardiac remodeling and delaying the progress of chronic heart failure.