Adaptive protection of the heart and stabilization of myocardial structures.

Adaptation of animals to short-term stress exposure (ASE) protected the heart against arrhythmias in acute ischemia and reperfusion and eliminated the decrease in threshold of fibrillation and arrhythmias is acute myocardial infarction and postinfarction cardiosclerosis. Cardioprotective effect of ASE was provided not only by the activation of GABAergic, opioidergic and cholinergic stress-limiting system but also by a mechanism formed at the level of heart itself. Isolated hearts of animals adapted to short-term stress exposure possessed a strikingly enhanced resistance to toxic doses of catecholamines, Ca2+, and to reperfusion damage following total ischemia. Contracture-inducing and arrhythmogenic effects of these factors and the release of CK into the perfusate were manifold reduced in ASE. Mitochondria and elements of SR Ca-pump isolated from the hearts of adapted animals were much more resistant to autolysis. This phenomenon of adaptive stabilization of structures (PhASS) was accompanied by the accumulation of HSP 71 and a simultaneous increase in the heart thermal stability. In the coronary artery ligation the PhASS lacked the anti-ischemic effect, but it provided a decrease of the necrotic zone by more than 40%, the ischemic zone being unchanged, due to its cytoprotective effect.