[Cardioprotective effects of adaptation to restraint stress and hypoxia]

Abstract

Isolated rat heart experiments have revealed that restraint stress adaptation results in enhanced resistance of the isolated heart to reperfusion. There is also a higher resistance to the autolysis of the organelles isolated from the hearts of stress-adapted animals. This complex of changes is designated as a phenomenon of adaptive stabilization of structures (PhASS). The phenomenon developing in restraint stress adaptation substantially limits arrhythmias, contracture, contraction amplitude depression, and creatine kinase release into the perfusate in thermal damage to the isolated rat heart. Simultaneously, PhASS is accompanied by a multiple increase in five hsp70 isoforms with pI 5.8-6.3 in cytosol and two isoforms with pI about 6.3 in the nucleoplasm. Only two hsp70 isoforms with pI about 5.8 accumulate solely in cytosol during adaptation to intermittent hypoxia. Consistently, the resistance of Ca(2+)-pump and nuclear DNA remains unchanged and the protection against reperfusion and thermal damage are several times less pronounced.