Abstract
Adaptation of rats to repetitive hypoxia leads to a decrease in the severity and frequency of arrhythmias induced by epinephrine. Naloxone abolishes antiarrhythmic effect of adaptation. Activation of μ-and δ-opioid receptors is one of the important factors mediating antiarrhythmic effect of adaptation. Intravenous administration of acetorphan, an enkefalinase inhibitor, produces statistically significant antiarrhythmic effect in the control group. Thus, the antiarrhythmic effect of hypoxic adaptation results from activation of μ-and δ-opioid receptors due to increased level of endogenous enkefalins.
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