[The phenomenon of the adaptive stabilization of cardiac structure and the protection of the heart].

It is known that adaptation to short-term repeated stress-effects may significantly increase human resistance to many factors; it may particularly prevent lethal cardiac fibrillation in the case of acute ischemia and reperfusion of the heart and limit the area of necrotized myocardium in the case of ischemia. The present investigations have shown that the mechanism responsible for this resistance improvement is related not only to neurohormonal factors but also to heart structures as such. Isolated hearts of adapted animals display substantially increased resistance to contractural and arrhythmogenic effects of ischemia and reperfusion, cardio-toxic doses of catecholamines and toxic concentrations of calcium. In all these situations, CPK loss, which is a quantitative characterization of the damage, diminishes as a result of adaptation. Analysis of this phenomenon shows that the structures isolated from hearts of adapted animals, i.e. Ca-pump of the sarcoplasmic reticulum and mitochondria, display a markedly greater resistance to autolysis during prolonged storage. Thus during adaptation to short-term repeated stress-effects the phenomenon of adaptation stabilization of cardiac structures develops at the organ level. This phenomenon is accompanied by an increase in the thermal stability of the heart. From this point of view the role of thermal stress proteins in the phenomenon of adaptation stabilization is discussed and the genetic mechanism underlying the phenomenon is described.