Rosen M R
J Am Coll Cardiol. 1985 May;5(5 Suppl A):22A-34A. doi: 10.1016/s0735-1097(85)80460-5.
The toxic effects of digitalis are attributable in part to poisoning of the enzyme Na+-K+ ATPase and in part to the interactions of digitalis with the sympathetic and parasympathetic nervous systems. Additional modifiers of the toxic effects of digitalis include the concentrations of ions such as K+ and Ca2+, the age of the subject and the extent and type of cardiac disease. At the cellular electrophysiologic level, digitalis toxicity is seen as a depolarization of the membrane with the occurrence--individually or simultaneously--of abnormalities of impulse initiation (including delayed afterdepolarizations and abnormal automaticity) and abnormalities of conduction. The afterdepolarizations result in triggered arrhythmias that differ partially in their characteristics of onset and termination from automatic and reentrant arrhythmias. The cellular electrophysiologic basis for these arrhythmias induced by toxic concentrations of digitalis and their implications with respect to arrhythmogenesis in the in situ heart are explored in detail.
洋地黄的毒性作用部分归因于Na+-K+ ATP酶中毒，部分归因于洋地黄与交感神经和副交感神经系统的相互作用。洋地黄毒性作用的其他影响因素包括K+和Ca2+等离子的浓度、受试者的年龄以及心脏病的程度和类型。在细胞电生理水平上，洋地黄毒性表现为膜去极化，并伴有冲动起始异常（包括延迟后除极和异常自律性）和传导异常的单独或同时出现。后除极导致触发型心律失常，其起始和终止特征与自律性和折返性心律失常部分不同。本文详细探讨了洋地黄中毒浓度诱导这些心律失常的细胞电生理基础及其对原位心脏心律失常发生机制的影响。
