Ducouret P
Br J Pharmacol. 1976 Jun;57(2):163-84. doi: 10.1111/j.1476-5381.1976.tb07465.x.
1 The action of quinidine sulphate 50 muM has been investigated on frog auricular trabeculae transmembrane currents recorded with a double sucrose gap apparatus. Results were obtained either in current or in voltage clamp conditions. 2 Quinidine modified the time course of repetitive activity elicited by long lasting depolarizing currents and reduced the range of current over which repetitive activity could be triggered, eventually abolishing repetitive responses altogether. 3 Several authors have emphasized the limitations of the voltage clamp method. Taking into account these limitations, the numerical values of the parameters obtained in the present work must not be considered as exact values but may be interpreted as indicators of the variations of the parameters. 4 The results are in agreement with previous findings that the main features of the action of quinidine are to produce (a) a reduced maximum rate of depolarization (MRD), (b) a reduced total amplitude of action potential, (c) a flattening of the plateau of the action potential, (d) a slight prolongation of the tail of the action potential, (e) an increased effective refractory period without greatly prolonging action potential duration, (f) no change of resting potential and of 50% repolarization time. 5 The analysis of ionic conductances has provided explanations for the above effects. 6 Quinidine reduced the reactivation kinetics of the sodium inward current, and decreased sodium conductance and the steady state of activation. These effects account for (a) and (b). 7 Quinidine increased the activation and inactivation time constants of sodium conductances, which account in part for (e). 8 Quinidine delayed reactivation of slow inward current, reduced calcium conductance, and decreased the steady state of activation of calcium conductance. These effects could account for (c). 9 The amplitudes of the two components of the delayed conductances responsible for repolarization were decreased by quinidine, and the time constant of activation for the faster of the two was slowed. These effects could account for (d) and in part for (e).
已使用双蔗糖间隙装置记录蛙心耳小梁跨膜电流，研究了50微摩尔硫酸奎尼丁的作用。结果是在电流钳或电压钳条件下获得的。
奎尼丁改变了由持久去极化电流引发的重复活动的时间进程，并减小了可触发重复活动的电流范围，最终完全消除了重复反应。
几位作者强调了电压钳方法的局限性。考虑到这些局限性，本研究中获得的参数数值不应被视为精确值，而可解释为参数变化的指标。
结果与先前的研究结果一致，即奎尼丁作用的主要特征是产生：(a) 最大去极化速率降低（MRD），(b) 动作电位总幅度降低，(c) 动作电位平台期变平，(d) 动作电位尾部略有延长，(e) 有效不应期增加而动作电位持续时间无明显延长，(f) 静息电位和50%复极化时间无变化。
离子电导分析为上述效应提供了解释。
奎尼丁降低了钠内向电流的再激活动力学，降低了钠电导和激活稳态。这些效应解释了(a)和(b)。
奎尼丁增加了钠电导的激活和失活时间常数，这部分解释了(e)。
奎尼丁延迟了慢内向电流的再激活，降低了钙电导，并降低了钙电导激活的稳态。这些效应可以解释(c)。
负责复极化的延迟电导的两个成分的幅度被奎尼丁降低，两者中较快成分的激活时间常数减慢。这些效应可以解释(d)，并部分解释(e)。
