Dobmeyer D, Muir W W, Schaal S F
J Cardiovasc Pharmacol. 1985 Mar-Apr;7(2):238-44. doi: 10.1097/00005344-198503000-00005.
We studied the electrophysiologic effects of flecainide on noninfarcted and infarcted dog hearts and in dogs anesthetized with halothane and administered intravenous epinephrine. Flecainide demonstrated no effect on atrial conduction times, but significantly (p less than 0.05) increased ventricular conduction times in noninfarcted, infarcted, and halothane-epinephrine-exposed dog hearts. Atrial and ventricular effective refractory periods (ERPs) were significantly (p less than 0.05) increased by flecainide. The increase in ERP was more pronounced in infarcted than in noninfarcted dog hearts. Flecainide significantly (p less than 0.05) decreased the echo zone for two or more repetitive ventricular responses in infarcted dog hearts and eliminated all ventricular arrhythmias observed at 48 h after coronary artery ligation. The dose of epinephrine required to induce ventricular arrhythmias in dogs anesthetized with halothane was significantly increased (p less than 0.05) by flecainide. Acute intravenous administration of flecainide to dogs with infarcted hearts produced sinus arrest, transient third-degree heart block, inability to pace, right bundle branch block, and torsade des pointes. Our results provide evidence that flecainide produces its antiarrhythmic effects by increased ventricular ERP and ventricular conduction time. Caution is advised when administering flecainide to patients with previous history of myocardial infarction.
我们研究了氟卡尼对未梗死和梗死犬心脏以及对用氟烷麻醉并静脉注射肾上腺素的犬的电生理作用。氟卡尼对心房传导时间无影响，但在未梗死、梗死以及暴露于氟烷 - 肾上腺素的犬心脏中显著（p小于0.05）增加了心室传导时间。氟卡尼显著（p小于0.05）增加了心房和心室有效不应期（ERP）。梗死犬心脏中ERP的增加比未梗死犬心脏更明显。氟卡尼显著（p小于0.05）减小了梗死犬心脏中两个或更多重复性心室反应的回声区，并消除了冠状动脉结扎后48小时观察到的所有室性心律失常。氟卡尼显著（p小于0.05）增加了用氟烷麻醉的犬诱发室性心律失常所需的肾上腺素剂量。对梗死心脏的犬急性静脉注射氟卡尼会导致窦性停搏、短暂性三度房室传导阻滞、无法起搏、右束支传导阻滞和尖端扭转型室速。我们的结果提供了证据表明氟卡尼通过增加心室ERP和心室传导时间产生抗心律失常作用。对有心肌梗死病史的患者使用氟卡尼时建议谨慎。
