@@ It has been reported that sevoflurane postconditioning can protect cardiomyocytes against hypoxia/reperfusion injury[1]. However, the mechanisms remains incompletely studied. Some researches reported that sevoflurane postconditioning had been mediated, at least in part, by the members of mitogen-activated protein kinases (MAPK) such as phosphatidylinositol-3-kinase (PI3K) and extracellular signal-regulated kinases 1/2 (ERK1/2) activation[2,3]. P38 MAPK is the third member of MAPK family. Whether p38 MAPK mediate the cardioprotective effect is still unclear. In this study we aimed to investigate the role of p38 MAPK pathway on sevoflurane postconditioning against hypoxia/reoxygenation injury in primarily cultured neonatal rats cardiomyocytes in vitro.