Summary: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 pendorphin in adrenal glands while stress-induced changes in 0-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 vasculanzation of the myocardial zone adjacent to the scar.
The phenomenon of adaptive stabilization of structures (PhASS) develops during adaptation of the organism to intermittent restraint stress. The PhASS manifests itself in a considerably increased resistance of the heart to a broad spectrum of harmful factors. In the present work, the content of hsp70 and their role in the development of PhASS during adaptation to intermittent restraint stress and to intermittent hypoxia were studied. In adaptation to restraint stress, five hsp70 isoforms with pI ranging from 5.7 to 6.3 were accumulated in the myocardium. The heart simultaneously became strikingly resistant to reperfusion paradox and heat shock. In adaptation to hypoxia, only two hsp70 isoforms with pI about 5.8 were accumulated. The resistance to reperfusion paradox was not increased and the resistance to heat shock was increased only moderately. These data suggest a role of different hsp70 isoforms in the mechanism of PhASS as well as adaptive protection of the heart.
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