Prevention and elimination of heart arrhythmias by adaptation to intermittent high altitude hypoxia.
It was shown that adaptation to intermittent hypoxia in altitude chamber prevented the poststress fall of the electrical threshold of heart fibrillation. In acute ischemia, the number of fibrillation episodes and the death rate of preadapted animals were 2-3 fold lower than in controls. The adaptation to hypoxia resulted in a significant increase in concentration of opioid peptide beta-endorphin in adrenal glands while stress-induced changes in beta-endorphin in brain structures of adapted animals were much less pronounced. In animals with postinfarction cardiosclerosis, the course of hypoxic actions resulted in restoration of the decreased heart fibrillation threshold, reduced the heart ectopic activity which had developed on the background of vagal bradycardia, and eliminated depression of the heart contractile function. Simultaneously, the adaptation induced a decrease of the postinfarction scar by one-third and an increase of vascularization of the myocardial zone adjacent to the scar.
D000222:Adaptation, Physiological; D000531:Altitude; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000517:prevention & control*; D001923:Brain Chemistry; D003327:Coronary Disease / Q000503:physiopathology; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology; D010100:Oxygen; D051381:Rats; D011919:Rats, Inbred Strains; D013312:Stress, Physiological / Q000503:physiopathology; D001615:beta-Endorphin / Q000032:analysis / Q000502:physiology
D001615:beta-Endorphin; D010100:Oxygen