Akiyama K, Hashimoto K
Department of Pharmacology, Yamanashi Medical College, Japan.
Jpn J Pharmacol. 1990 Aug;53(4):419-26. doi: 10.1254/jjp.53.419.
Triggered activity due to delayed after depolarization has been postulated to be one of the generation mechanisms of some arrhythmias, especially that due to digitalis toxicity. The present experiment demonstrates an in vivo canine model of ventricular arrhythmias that were triggered by ventricular stimulation during administration of low doses of ouabain. Ventricular ectopic beats could be induced by stimulation before the occurrence of spontaneous ventricular arrhythmia, and the coupling interval of the first ectopic beat was shortened as the stimulation rate increased. Verapamil (0.2 mg/kg, i.v.) was ineffective in suppressing the occurrence of the triggered ventricular ectopic beats, but lidocaine (1 and 3 mg/kg, i.v.) and disopyramide (0.3 and 1 mg/kg, i.v.) were effective in suppressing these digitalis-induced triggered ventricular ectopic beats in a dose-dependent fashion.
由于延迟后除极引起的触发活动被认为是某些心律失常的发生机制之一，尤其是洋地黄毒性所致的心律失常。本实验展示了一种体内犬室性心律失常模型，该模型是在给予低剂量哇巴因期间通过心室刺激触发的。在自发性室性心律失常发生之前，刺激可诱发室性早搏，且随着刺激频率增加，第一个早搏的联律间期缩短。维拉帕米（0.2mg/kg，静脉注射）对抑制触发的室性早搏无效，但利多卡因（1和3mg/kg，静脉注射）和丙吡胺（0.3和1mg/kg，静脉注射）能以剂量依赖的方式有效抑制这些洋地黄诱导的触发室性早搏。
