Ginsenosides, one of the well-known traditional herbal substance, frequently are used in South Korea for the prevention of cardiovascular disease. The effects of ginsenoside-Re (G-Re) on ischemia-induced heart were investigated through analyses of hemodynamic change including perfusion pressure, aortic flow, coronary flow, and cardiac output. Myocardial function was recorded. Administration of ginsenoside-Re significantly prevented decreases in perfusion pressure, aortic flow, coronary flow, and cardiac output. The Administration of G-Re significantly recovered all of the hemodynamic parameters, except heart rate, after ischemia-reperfusion (I/R) injury (perfusion pressure: 78.49±3.98% vs. 66.61±3.3%, aortic flow volume: 59.26±2.29% vs. 42.68±2.17%, coronary flow volume: 74.89±2.88% vs. 52.89±2.81%, and cardiac output: 63.12±3.81% vs. 45.25±3.83%, P⁄0.01, respectively, normal control as 100%). The intracellular calcium ([Ca 2+ ] i ) content in cardiomyocytes was quantitatively determined. Administration of G-Re significantly prevented [Ca 2+ ] i increase that had been induced by simulated I/R in vitro (P⁄0.01) in a dose-dependent manner, suggesting that the antiischemic role of G-Re is mediated by the inhibition of [Ca 2+ ] i increase.Over all, we found that the administration of G-Re has cardioprotective effects on the isolated heart. The beneficial effects may be mediated through controlling the level of [Ca 2+ ] i . These results indicate that G-Re has a distinct cardioprotective effect in an isolated rat heart.The primary cause of death worldwide 1,2 is ischemic cardiac disease (ICD). Myocardial infarction (MI) is the manifestation of a cardiac injury following coronary occulsion. When an MI is cured with early revascularization, this conditions leads to cardiac reperfusion. ischemia-reperfusion (I/R) is related with myocardial ischemia. When coronary flow is restored, the harmful effects occur causing oxidative stress and intracellular calcium increase, which lead to cell death 3 .The primary evidence of cardiac I/R are myocyte death and contractile dysfunction 4-6 . Individual surviving an MI are susceptible to cardiac dysfunction and sudden death 7 . During the last three decades, many development has been made in the cure of cardiac infarction, and these progress have decreased death from ICD 8-10 . While I/R injury limits cardiac salvage, reperfusion therapies that are protective in animal heart models have not yet been many advanced 11 . However, many mechanisms have been proposed that may relate cardiac I/R injury. Intracellular Ca 2+ ([Ca 2+ ] i ) is a important signal for controlling cellular functional level, including cellular survival and death 12 . While a small amount of [Ca 2+ ] i is need for optimal cellular function, showing obvious evidence suggests that an increased cytosolic Ca 2+ is one of the major contributors to car-