[Effect of heme oxygenase-1 expression and activity on the heart function in ischemia-reperfusion].
The purpose of this study was to determine the protective effects of heme oxygenase-1 (HO-1) expression against postischemic myocardial dysfunction. We also investigated HO-1 expression in cardiac tissue from the left and right ventricles of myocardium. Rat hearts were isolated and perfused according to Langendorff technique to evaluate the recovery of myocardial function after 20 min of global ischemia and 40 min of reperfusion. We found that HO-1 expression was more expressed in left ventricles of myocardium in basic conditions and after ischemia/reperfusion as well as after its previous induction by hemin. Upregulation of the inducible isoform of HO-1 and increase its activity after treatment of animals with hemin 24 h before ischemia ameliorated myocardial function (raised left ventricular developed pressure, decreased end-diastolic pressure, attenuated vasoconstriction) and reduced oxydative stress in cardiac tissue during reperfusion of isolated hearts. Zinc protoporphyrin IX, an inhibitor of heme oxygenase activity, completely abolished the HO-1 expression in left ventricles of myocardium and increased postischemic myocardial dysfunction. Likewise, cardiac tissue injury was exacerbated by treatment with zinc protoporphyrin IX through significant inhibition of HO activity and increasing of hydroxyl radical production on reperfusion. The treatment of animals with hemin and following ischemia/reperfusion resulted in 5-6-times increase of HO-1 expression in the left ventricle of myocardium whereas in right ventricle only in 3-times. Our data provide strong evidence for a primary role of HO-1 in cardioprotection against reperfusion injury and show different HO-1 expression in left and right ventricles of myocardium.
T V
TV
Kukoba
A V
AV
Kotsiuruba
O O
OO
Moĭbenko
D000818:Animals; D003326:Coronary Circulation / Q000502:physiology; D006321:Heart / Q000503:physiopathology*; D006419:Heme Oxygenase (Decyclizing) / Q000096:biosynthesis* / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D051381:Rats; D016276:Ventricular Function / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology
D006419:Heme Oxygenase (Decyclizing); C491523:Hmox1 protein, rat