Coetzee W A, Opie L H, Saman S
Department of Medicine, University of Cape Town, Observatory, South Africa.
J Mol Cell Cardiol. 1987 Oct;19 Suppl 5:13-21. doi: 10.1016/s0022-2828(87)80606-5.
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.
延迟后除极（DADs）是依赖钙离子的电生理异常现象，由多种导致细胞内钙离子超载的情况诱发，包括快速起搏、异丙肾上腺素、二丁酰环磷腺苷以及细胞内注射钙离子。由于怀疑钙离子超载在缺血和再灌注细胞损伤中均起作用，一个合理的假设是DADs可能在缺血或再灌注心律失常中起作用。然而，尚未获得关于DADs起这种作用的直接证据。我们提出，只要有ATP形式的能量可用，DADs可能与心律失常相关，在这些心律失常中，存在足够程度的钙离子超载，导致肌浆网（SR）中钙离子的振荡释放增加。钙离子的持续增加可能反映能量耗竭，因此排除了DADs对心律失常发生的显著贡献。因此，与能量明显耗竭的严重缺血相比，DADs更有可能在以下情况中起作用：（i）再灌注心律失常和（ii）中度缺血组织中出现的心律失常。
