Ferrier G R
Prog Cardiovasc Dis. 1977 May-Jun;19(6):459-74. doi: 10.1016/0033-0620(77)90010-x.
Digitalis-induced OAP provide a mechanism of automaticity that may be responsible for many arrhythmias induced by cardiac glycosides. In response to digitalis, OAP occur in tissues of the specialized conducting systems of both ventricles and atria and, under the influence of tension, occasionally in ventricular myocardium. Digitalis, in toxic doses, suppresses "normal" pacemaker activity possibly in part by enhancing overdrive suppression. In contrast to "normal" pacemaker activity, OAP exhibit, both in magnitude and rate of depolarization, postpacing acceleration. This plus the coupled nature of OAP are important characteristics in the generation of complex arrhythmias by OAP. Conduction disturbances may also be related to OAP. At early stages of intoxication OAP may speed conduction of superimposed beats relative to earlier or later beats. More advanced stages of intoxication are associated with conduction block. The occurrence of digitalis-induced OAP is promoted by high concentrations of calcium, low concentrations of potassium, and moderate stretch. OAP can be suppressed by high concentrations of potassium, reduction of extracellular calcium, and exposure to antiarrhythmic agents including diphenylhydantoin, verapamil, and aprindine. The effectiveness of the latter two agents may be related to ability to block transmembrane calcium currents. Digitalis-induced OAP in atrial tissue can be abolished by acetylcholine. A transmembrane current possibly but not necessarily carried by calcium appears to underly the occurrence of OAP. This current demonstrates kinetic properties different from those of the slow inward current associated with the plateau of the cardiac action potential. Calcium is intimately involved in the mechanism causing OAP and may be responsible for aftercontractions observed in conjunction with OAP. Aftercontractions greatly affect contractility and may be responsible at least in part for some of the inotropic actions of digitalis. Thus the occurrence of OAP may be linked to the inotropic actions of digitalis. Digitalis-induced OAP provide a mechanism of automaticity with characteristics paralleling automatic behavior observed in intact animals intoxicated with digitalis. The relative importance of OAP in the genesis of clinically important arrhythmias awaits further investigation.
洋地黄诱导的迟后除极提供了一种自律机制,可能是许多强心苷诱发心律失常的原因。对洋地黄的反应中,迟后除极发生在心室和心房的特殊传导系统组织中,在张力影响下,偶尔也发生在心室肌中。中毒剂量的洋地黄可能部分通过增强超速抑制来抑制“正常”起搏活动。与“正常”起搏活动相反,迟后除极在去极化幅度和速率上均表现出起搏后加速。这一点加上迟后除极的耦联特性是迟后除极产生复杂心律失常的重要特征。传导障碍也可能与迟后除极有关。在中毒早期,迟后除极可能使叠加搏动相对于更早或更晚的搏动传导加速。中毒更严重阶段则与传导阻滞有关。高钙浓度、低钾浓度和适度牵张会促进洋地黄诱导的迟后除极的发生。高钾浓度、细胞外钙减少以及暴露于包括苯妥英钠、维拉帕米和茚满丙二胺在内的抗心律失常药物可抑制迟后除极。后两种药物的有效性可能与阻断跨膜钙电流的能力有关。乙酰胆碱可消除心房组织中洋地黄诱导的迟后除极。一种可能但不一定由钙携带的跨膜电流似乎是迟后除极发生的基础。这种电流表现出与与心脏动作电位平台期相关的缓慢内向电流不同的动力学特性。钙密切参与导致迟后除极的机制,可能是与迟后除极相关的后收缩的原因。后收缩极大地影响收缩力,可能至少部分是洋地黄某些正性肌力作用的原因。因此,迟后除极的发生可能与洋地黄的正性肌力作用有关。洋地黄诱导的迟后除极提供了一种自律机制,其特征与在洋地黄中毒的完整动物中观察到的自动行为相似。迟后除极在临床上重要心律失常发生中的相对重要性有待进一步研究。