[Enhanced resistance of the heart to arrhythmogenic factors as affected by adaptation of the body to stress exposures].

Adaptation to short-term nondamaging stress effects largely limits or prevents cardiac arrhythmias in acute ischemia and reperfusion. The study examines to what extent this anti-arrhythmic effect depends on adaptational shifts of the heart itself. Isolated hearts of animals adapted to stress are shown to possess dramatically increased resistance to arrhythmias induced by local ischemia and reperfusion. The role of activated prostaglandin biosynthesis, adenosine, antioxidant systems, desensitization and other protective control systems functioning at heart level to provide this anti-arrhythmic effect is discussed.