AIMWhether hemin, a heme oxygenase 1 (HO-1) inducer, reduces ischemia/reperfusion injury and whether NO synthase (NOS) and PKC are involved in the cardioprotective effects were investigated in the present study.

METHODSThe Langendorff model of isolated rat heart was used. The ventricular function, infarct size, LDH and CK during ischemia/reperfusion period were also observed.

RESULTS(1) After intraperitoneal injection of hemin (50 mg/kg) for 24 h, COHb concentration in rat blood enhanced. He-min preconditioning prevented the increase in LVEDP, decrease in LVDP and +/- dP/dt(max) in the isolated ischemia/reperfusion (ischemia for 30 main and subsequent reperfusion for 2 h) rat hearts. The leakage of LDH and CK in the coronary effluent was significantly declined in hemin-treated rat hearts. And the infarct size was als reduced. (2) By using an inhibitor of NOS NG-nitro-L-arginine methyl ester before the administration of hemin could inhibit the protection induced by hemin. (3) Administration of an inhibitor of protein kinase C chelerythrine (1 mg/kg) before hemin preconditioning could also abolish the cardioprotection induced by hemin.

CONCLUSIONThese data suggest that the involvement of NO synthase and protein kinase C have been implicated in hemin-induced delayed cardioprotection in isolated rat hearts.