Huerta F, Santamaria R, Pourrias B
Arch Int Pharmacodyn Ther. 1984 Feb;267(2):289-98.
The electrophysiological effects of carocainide (770207) were assessed in "in vivo" and "in vitro" experiments on dogs' hearts. Intravenous administration of 5 mg/kg body weight of carocainide significantly lengthened the following: A-H interval, the shortest atrial pacing cycle length maintaining 1:1 atrioventricular (A-V) nodal conduction, H-V interval, left bundle-ventricle (LB-V) interval, the shortest His bundle pacing cycle length maintaining 1:1 His-Purkinje conduction, QRS duration, right atrial and right ventricular effective refractory periods. In Purkinje fiber-papillary muscle junction preparations driven at a constant cycle length of 1000 msec, perfusion of carocainide at the concentration of 1.25 10(-5) M and 2.5 10(-5) M, increased conduction time between Purkinje and muscle fibers and decreased the rate of depolarization of Purkinje fibers and papillary muscle. These results suggest that carocainide depresses conduction and lengthens refractory periods at atrial and ventricular levels and provide an explanation for the positive effect of this compound against experimental cardiac arrhythmias.
在犬心脏的“体内”和“体外”实验中评估了卡罗卡尼（770207）的电生理效应。静脉注射5mg/kg体重的卡罗卡尼可显著延长以下指标：A-H间期、维持1:1房室（A-V）结传导的最短心房起搏周期长度、H-V间期、左束支-心室（LB-V）间期、维持1:1希氏束-浦肯野传导的最短希氏束起搏周期长度、QRS时限、右心房和右心室有效不应期。在以1000毫秒恒定周期长度驱动的浦肯野纤维-乳头肌连接标本中，灌注浓度为1.25×10⁻⁵M和2.5×10⁻⁵M的卡罗卡尼，可增加浦肯野纤维与肌纤维之间的传导时间，并降低浦肯野纤维和乳头肌的去极化速率。这些结果表明，卡罗卡尼可抑制心房和心室水平的传导并延长不应期，这为该化合物对实验性心律失常的积极作用提供了解释。
