Objective To investigate the effect of vitamin E (VE) on myocardium in a rat model of renalischemia reperfusion (RIR). Methods Rats were divided into three groups: a control group, RIR model group, andexperimental (VE + RIR) group fed with VE for 4 weeks before the RIR model was prepared. Contents of malondialdehyde(MDA), myeloperoxidase (MPO), xanthine oxidase (XO), superoxide dismutase (SOD), and nitric oxide (NO) weremeasured in the myocardium. In addition, levels of creatine kinase (CK) and creatine kinase MB isoenzyme (CK-MB) inplasma were determined. Mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rise rate ofleft ventricular pressure ( dP/ dt_max ) and maximal fall rate of left ventricular pressure (-dP/ dt_max ) were monitored.Myocardial cell morphology and expression of endothelial nitric oxide synthase (eNOS) were observed by light microscopyand immunohistochemistry. Western blot analysis was conducted to quantify P47phox expression in cardiomyocytes. Results Compared with the control group, levels of MDA, MPO, XO, and NO were increased, and the level of SOD wasdecreased in the myocardium of RIR group rats; moreover, CK and CK-MB plasma levels were increased in this group.Compared with the control group, values of MAP, LVSP, dP/ dt_max, and -dP/ dt_max were obviously decreased in the RIRgroup. In addition, aggravation of myocardial damage, number of eNOS-positive cells, and P47phox protein expression wereincreased in the RIR group compared with the control group. Compared with RIR group, the VE + RIR group exhibiteddecreased levels of MDA, MPO, and XO, as well as increased levels of SOD increased in myocardium. In addition, plasmalevels of CK and CK-MB were decreased, NO content was increased, and values of MAP, LVSP, dP/ dt_max, and -dP/ dt_maxwere obviously increased in the VE + RIR group compared with the RIR group. Moreover, compared with the RIR group,microscopic cardiomyocyte injury was reduced, numbers of eNOS-positive cells were increased, and P47phox proteinexpression was decreased in the VE + RIR group. Conclusions VE potentially protects the myocardium from RIR by antiinflammatoryand anti-oxidative mechanisms, as well as by increasing NO content and decreasing P47phox protein expression.