Proposed role of energy supply in the genesis of delayed afterdepolarizations--implications for ischemic or reperfusion arrhythmias.
Delayed afterdepolarizations (DADs) are Ca++-dependent electrophysiological abnormalities, which are evoked by a variety of conditions that induce intracellular Ca++ overload, including fast pacing, isoproterenol, dibutyryl cyclic AMP, and intracellular injection of Ca++. Since Ca++ overload is suspected of playing a role in both ischemic and reperfusion cellular damage, a reasonable hypothesis would be that DADs could play a role in ischemic or reperfusion arrhythmias. No direct proof has, however, been obtained for such a role for DADs. We propose that DADs could be associated with arrhythmias in which there is Ca++ overload of sufficient magnitude to cause an increased oscillatory release of Ca++ from the sarcoplasmic reticulum (SR), provided energy is available in the form of ATP. A sustained increase of Ca++ is likely to reflect energy depletion and therefore exclude a significant contribution of DADs to arrhythmia development. Thus, DADs are more likely to play a role in: (i) reperfusion arrhythmias and (ii) arrhythmias arising in moderately ischemic tissue, than in severe ischemia with marked energy depletion.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D003326:Coronary Circulation; D003327:Coronary Disease / Q000150:complications*; D004734:Energy Metabolism; D006168:Guinea Pigs; D006329:Heart Conduction System / Q000503:physiopathology; D007473:Ion Channels / Q000378:metabolism*; D009200:Myocardial Contraction; D010210:Papillary Muscles / Q000502:physiology
D007473:Ion Channels; D002118:Calcium