Oxidative stress plays a major role in causing reperfusion injury following prolonged ischemia. CAPE has been shown to have antioxidant, anti-inflammatory, and cardioprotective effects following regional myocardial ischemia/reperfusion injury. The effects and mechanisms of CAPE in global myocardial I/R injury are still unclear. In this study, CAPE was tested in isolated perfused rat hearts following global I (30 min)/R (60 min). We recorded left ventricular developed pressure (LVDP), left ventricular end systolic pressure (LVESP), the peak of the first derivative of left ventricular pressure (dP/dtmax), and infarct size. We found that untreated I/R hearts (n=11) recovered LVDP to 45 ± 8% (p<0.05), LVESP to 106 ± 7% (p<0.05), and dP/dtmax to 33 ± 5% (p<0.05) of baseline values, respectively, at the end of 60 minutes reperfusion. By contrast, CAPE (40 mM, n=6) given at reperfusion for 5 minutes significantly restored LVDP to 75 ± 15%, LVESP to 133 ± 13%, and dP/dtmax to 54 ± 12% of baseline values, respectively (all p<0.05). Moreover, CAPE also significantly reduced infarct size to 19 ± 2% (n=6) compared to