ADAPTATIVE PROTECTION OF THE HEART AGAINST ARRHYTHMIAS Institute of General AND NECROSIS. F.Z. Meerson. Pathology and Pathological Physiology of the USSR AMS, Moscow, USSR. Adaptation (A) of rats to repeated short-term stress exposure significantly limited durations of ventricular tachycardia and ventricular fibrillation (VF) in acute ischemia and reperfusion and eliminated the decrease in threshold of VF and arrhythmias in acute myocardium infarction and postinfarction cardiosclerosis. It was shown that the cardioprotective effect of A was provided not only by the activation of GABA-ergic, opioidergic and cholinergic stress-limiting systems but also by another mechanism formed at the level of the heart itself. It was established that isolated hearts of adapted animals possessed a strikingly enchanced resistance 2+ to toxic doses of catecholamines and Ca and to total ischemia and subsequent reperfusion. Contracture-induced and arrhythmogenic effects of these factors and the release of creatine phosphokinase into the perfusate were manifold reduced in A as compared to the control. Mitochondia and elements of the sarcoplasmic reticulum Capump isolated from the hearts of adapted animals were much more resistant to autolysis in a prolonged storage. This fact was designated as the phenomenon of adaptive stabilisation of structures (PASS). It was proved that the PASS formation in A was accompanied by an accumulation of HSP with molecular weight 70 kDa at a simultaneous increase in the heart thermal stability. The PASS lacked the anti-ischemic effect in the coronary artery ligation but it provided a decrease of the necrotic zone by more than 40% due to its cytoprotective effect. The general biologic significance of the PASS is discussed.