Abstract: AIM:To investigate the effect of pyruvate on myocardial ischemia/reperfusion (I/R) injury and the underlying mechanism. METHODS: The animal model of myocardial I/R injury was induced by 30 min of left anterior descending coronary occlusion followed by 2 h of reperfusion. Thirty rats were randomly divided into three groups: sham group, I/R group and I/R plus pyruvate treatment (I/R+Pyr) group. Pyruvate was intravenously infused at 25 mg/(kg·h) for 2 h, 5 min before reperfusion. Hemodynamic parameters (including LVSP, MABP and ±LV dP/dtmax) phosphorylation and total levels of JNK were determined and cardiomyocyte apoptosis was evaluated by TUNEL staining. RESULTS: LVSP, MABP and ±LV dP/dtmax decreased in I/R group and pyruvate treatment reversed these effects. p-JNK level increased in I/R group compared with that in sham group. Pyruvate inhibited p-JNK activation but did not change JNK expression. The index of apoptotic cardiomyocytes decreased with pyruvate treatment compared with that in I/R group. CONCLUSION: Pyruvate improves the myocardial function and inhibits myocardial apoptosis, which may result from the inhibition of JNK phosphorylation in the rat myocardial I/R model.