[The role of cholinergic regulation and stabilization of myocardial structures in the adaptive protection of the heart].

It was found that rat immobilization in small-size cages leb to physiological changes. On day 1 it was a stress-reaction that resulted in decreases of the fibrillation threshold and arrhythmia resistance. On day 5 it was an increase in the vagal tone that caused noticeable atropine-relieved bradycardia. The fibrillation level returned to the baseline. Heart resistance to ischemic and reperfusion arrhythmias increased drastically as compared to the control level. On day 15 the vagal effect declined to reach the baseline; in spite of this heart tolerance to reperfusion arrhythmias further increased. This was followed by enhanced resistance of isolated hearts of the adapted animals to the reperfusion paradox and tonic concentrations of epinephrine and Ca2+, which indicated the formation of the phenomenon of adaptation stabilization of cardiac structures. After termination of the 5-day stressogenic exposure the cholinergic stress-limiting protection of the heart disappeared rapidly, i. e. within 12 hours. The protective effect of the adaptation stabilization phenomenon, which developed during 15 days of the stressogenic exposure, proved to be more stable and persisted during 15 days after its cessation. It is concluded that, based on the coordination of short-term central and long-term cellular mechanisms, the animal body develops optimal adaptation that emerges rapidly and persists for an adequately long period of time. The step-by-step replacement of central mechanisms with cellular ones provides high reliability and efficiency of the protection of the heart and the entire body from extended environmental effects.