Objective:To study cardioprote ctive effects and mechanisms of SEA0400(2-4-(2

5-difluorophenyl)methoxy-5-ethoxy aniline) on ischemia-reperfusion injury in rat myocytes.Methods:Rat myocyte suspension were obtained from adult rat hearts by Langendorff perfusion and enzymatic dissociation

and randomly divided into three groups including the control group

ischemia-reperfusion injury group and SEA0400 intervention group.The control group was incubated in normal condition for 60 minutes.The ischemia-reperfusion injury group underwent ischemia for 30 minutes and reperfusion for 30 minutes respectively.SEA0400 intervention group underwent the same as ischemia-reperfusion injury group in the presence of 1μmol/L SEA0400.MTT was applied for the measurement of the cardiomyocyte viability at the end of reperfusion period.The intracellular Ca2+ concentration was measured by laser scanning confocal microscope(LSCM)and expressed as fluorescence intensity of Fluo-3.Results:Ischemia-reperfusion resulted in the decrease of the cardiomyocyte viability and the increase of the fluorescence intensity of Fluo-3 in rat myocyte.SEA0400 could significantly increase the cardiomyocyte viability and decrease the fluorescence intensity of Fluo-3 in rat myocyte.Conclusion:SEA0400 could attenuate Ca2+ overload in cardiomyocytes and improve significantly the cardiomyocyte viability during ischemia and reperfusion periods.