The purpose of this study was to determine the protective effects of heme oxy-genase-1 expression against postischemic myocardial dysfunction. Isolated rat hearts were perfused according to the Langendorff technique with 20 min of global ischemia and 40 min of reperfusion. We found that HO-1 expression was more expressed in left ventricles of myocardium as well in basic conditions as after ischemia/reperfusion and previous induction by hemin. Upregulation of HO-1 and increasing its activity by hemin 24 h before ischemia ameliorated myocar-dial function (raised LVDP, decreased EDP, attenuated vasoconstriction) and reduced oxidative stress in cardiac tissue. Zinc protoporphyrin IX completely abolished the HO-1 expression in left ventricles of myocardium and increased postischemic myocardial dysfunction through significant inhibition of HO activity and increasing of hydroxyl radical production on reperfusion. The treatment of animals with hemin and following ischemia/reperfusion provided 5 or 6-fold in-creasing of HO-1 expression in left ventricles of myocardium whereas in right ventricles this rising was only 3-fold. Our data show different levels of HO-1 expression in left and right ventricles of myocardium and provide evidence for a primary role of HO-1 in cardioprotection against reperfusion injury.