[Primary stress-induced myocardial injury and cardiac arrhythmia. Part II]

1. Heart injuries in single severe stress manifesting themselves primarily in disturbances of membrane lipid bilayer, sarcolemmal Na, K-pump and sarcoplasmic Ca-pump. At the same time there appear limited disturbances of the heart energy supply, namely, of creatine kinase system and glycolysis system. These disturbances cause small-focal myocardial lesions, lead to disorders of myocardium stretchability (poststress rigidity) and reduce the cardiac electrical stability: fibrillation threshold falls and ectopic activity increases. This complex of injuries is reversible to a considerable extent, but in repeated stress, the above mentioned damages localized mainly in richly innervated conduction system accumulate to cause even more pronounced disturbances of electric stability and severe arrhythmias. 2. Severe stress and beta-adrenergic effects on the heart regularly result in coronary vasodilation and increased coronary blood flow. However, the entire primary complex of stress-induced injuries and disturbances of the heart electric stability occur in this process despite the increased coronary blood flow. This corresponds to a well-known fact that isoproterenol, a selective beta-agonist, dilates blood vessels and simultaneously provokes a complex of injuries in the heart similar to the stress-induced one. Thus beta-adrenergic stress-induced injuries may indeed develop as primary stress damage to cardiomyocytes without any relation to ischemia. 3. The main factor determining a high vulnerability or, on the contrary, resistance of the heart to stress is the state of stress-limiting systems, namely, opioidergic, GABAergic, cholinergic, adenosinergic and other ones. Activation of these systems by adaptation to repeated stress or some other factors prevents serious injuries of the heart in severe stress.(ABSTRACT TRUNCATED AT 250 WORDS)