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[Protective action of ethylglutathione at hypoxia-reoxygenation of the heart: role of glucose].

Glutathione is the main redox buffer in cardiomyocytes. The action of ethylglutathione possessing antioxidant properties on functional disorders evoked by 30-minute hypoxia of the isolated rat heart with subsequent reoxygenation has been studied. In control experiments, the presence of glucose (11 mM) in hypoxic perfusate was associated with lesser hypoxic contracture of the myocardium but also with the development of arrhythmias in all experiments, including ventricular tachycardias and fibrillation that may be due to arisen myocardial heterogeneity. After reoxygenation, a half of hearts in this group demonstrated inability to reproduce high rate of stimulation. These alterations were almost completely prevented when ethylglutathione (0.2 mM) was added into hypoxic perfusate. Its presence in the solution also facilitated 1.5-fold improvement of cardiac function recovery after reoxygenation. The results suggest that the protective action of ethylglutathione may be due to a reduced oxidative modification of ionic transport proteins. At non-glucose hypoxic perfusion, myocardial contracture was higher but abovementioned functional disorders did not arise, and ethylglutathione addition was inefficient.