Role of Opiate Receptors and ATP-Dependent Potassium Channels of Mitochondria in the Formation of Myocardial Adaptive Resistance to the Arrhythmogenic Effect of Ischemia and Reperfusion |
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Authors: | Yu B Lishmanov N V Naryzhnaya A B Krylatov L N Maslov S A Bogomaz D S Ugdyzhekova G J Gross J B Stefano |
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Institution: | (1) Tomsk Research Center, Siberian Division, Russian Academy of Medical Sciences, Institute of Cardiology, ul. Kievskaya 111a, Tomsk, 634050, Russia;(2) Tomsk State University, pr. Lenina 49, Tomsk, 634050, Russia;(3) Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin, United States;(4) Department of Surgery, State University of New York, United States |
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Abstract: | Preliminary stimulation of opiate receptors (ORs) by intravenous administration of agonist DALDA (0.5 mg/kg), 1 agonist DPDPE (0.5 mg/kg), and agonist (-)-U-50.488 (1 mg/kg) increases rat myocardial resistance to arrhythmogenic effect of coronary occlusion (10 min) and reperfusion (10 min). Activation of 2 ORs (DSLET, 0.5 mg/kg) has no effect on the incidence rate of ischemic and reperfusion arrhythmias. Preliminary administration of glibenclamide (0.3 mg/kg), an inhibitor of KATP channels, blocks the antiarrhythmic effect of DALDA and DPDPE. Repeated short-term exposures of rats to immobilization within two weeks increases the heart tolerance to the arrhythmogenic effect of coronary occlusion and reperfusion. This effect disappears after administration of CTAP (0.5 mg/kg), a antagonist, or injection of 5-hydroxydecanoate (5 mg/kg), an inhibitor of mitochondrial KATP channels. The selective antagonists of and ORs have no effect on cardiac adaptation-induced resistance to the arrhythmogenic effect of ischemia and reperfusion. We believe that stimulation of , , and ORs increases myocardial tolerance to the arrhythmogenic effect of ischemia and reperfusion through activation of KATP channels. The antiarrhythmic effect of the adaptation is mediated by stimulation of ORs and mitochondrial KATP channels. |
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