Dennis P D, Vaughan Williams E M
Br J Pharmacol. 1985 May;85(1):11-9. doi: 10.1111/j.1476-5381.1985.tb08825.x.
Intracellular potentials were recorded from rabbit atria, cardiac Purkinje cells and papillary muscles before and after exposure to various concentrations of indecainide. The effects of aprindine also were studied in the atrial preparations. Both drugs depressed the maximum rate of depolarization (MRD) in a dose-related manner, indecainide being approximately ten times more potent than aprindine. Aprindine caused a dose-related bradycardia, but indecainide had no significant effect on sinus node frequency. Indecainide had a dose-related negatively inotropic effect in normal, half-normal and twice-normal extracellular calcium concentrations. Indecainide shortened action potential duration (APD) in atrium and Purkinje cells but prolonged APD to 50% repolarization in ventricular muscle. The actions of indecainide were extremely persistent. No significant recovery of MRD was observed after pauses in stimulation of up to 16 s. Indecainide had no effect on effective refractory period (ERP) measured by interpolated premature stimuli. Indecainide is therefore categorized as a Class 1c antiarrhythmic agent. The effects of both aprindine and indecainide on MRD were increased in hypoxic atria. Conduction velocity in hypoxic atria exposed to indecainide was greater than in controls, however, suggesting the possibility of improved cell-to-cell coupling.
在暴露于不同浓度的茚满卡因前后，记录了兔心房、心脏浦肯野细胞和乳头肌的细胞内电位。还在心房标本中研究了阿普林定的作用。两种药物均以剂量相关的方式降低最大去极化速率（MRD），茚满卡因的效力约为阿普林定的十倍。阿普林定引起剂量相关的心动过缓，但茚满卡因对窦房结频率无显著影响。在正常、半正常和两倍正常的细胞外钙浓度下，茚满卡因具有剂量相关的负性肌力作用。茚满卡因缩短心房和浦肯野细胞的动作电位持续时间（APD），但使心室肌的APD延长至复极化50%。茚满卡因的作用极为持久。在长达16秒的刺激暂停后，未观察到MRD有明显恢复。茚满卡因对通过插入性早搏刺激测量的有效不应期（ERP）无影响。因此，茚满卡因被归类为1c类抗心律失常药物。在缺氧心房中，阿普林定和茚满卡因对MRD的作用均增强。然而，暴露于茚满卡因的缺氧心房中的传导速度大于对照组，这表明细胞间偶联可能得到改善。
