Oxidative stress has been implicated in the pathophysiology of myocardial ischemia/reperfusion (I/R) injury. The present study examined the hypothesis that (-)-epigallocatechin gallate (EGCg), a green tea extract, reduces the I/R-induced myocardial injury in animal model. The effects of EGCg on I/R-induced cell necrosis or apoptosis and generation of lipid peroxidation products in addition to cardiac hemodynamic variables were evaluated. We also assessed the effect of N-acetylcysteine (NAC) as an antioxidant for the positive control. Thirty minutes before undergoing 1 hour ligation of the anterior ventricular coronary artery, a single bolus of physiologic saline (control group) or NAC (150 mg/kg), or EGCg (15 mg/kg) was administered into the rabbit. Reperfusion was achieved by releasing the occlusion and restoring blood circulation for 3 hours. The results showed that the infarct size of the area at risk in NAC (36.90 짹 8.04%) or EGCg (38.48 짹 7.38%) pretreated rabbit hearts was significantly smaller than that in control (58.31 짹 13.87%). At the end of reperfusion, the serum level of troponin I in NAC (20.17 짹 4.50 ng/ml) or EGCg (23.64 짹 5.97 ng/ml) pretreated group was also significantly lower than that in control (38.15 짹 10.65 ng/ml). Cardiac hemodynamic data revealed that the left ventricular end-diastolic pressure of pretreated hearts with NAC or EGCg was lower than that of the control group at the end of reperfusion. The pretreatment of NAC or EGCg reduced not only the plasma level of lipid peroxidation products such as malondialdehyde (NAC group, 13.82 關M to 12.34 關M; EGCg group, 11.57 關M to 10.50 關M) and 4-hydroxynonenal (NAC group, 12.84 關M to 11.80 關M; EGCg group, 10.58 關M to 9.51 關M) but also reduced the number of I/R-induced apoptotic cells. In summary, the pretreatment of EGCg effectively reduced I/R-induced myocardial injury in the rabbit experimental model, which was proved by hemodyamically, biochemically, and morphologically.