ROLE OF CALCIUM-IONS IN TRANSIENT INWARD CURRENTS AND AFTER CONTRACTIONS INDUCED BY STROPHANTHIDIN IN CARDIAC PURKINJE-FIBERS
ROLE OF CALCIUM-IONS IN TRANSIENT INWARD CURRENTS AND AFTER CONTRACTIONS INDUCED BY STROPHANTHIDIN IN CARDIAC PURKINJE-FIBERS
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DOI：
10.1113/jphysiol.1978.sp012416
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发表时间：
1978-01-01
影响因子：
5.5
通讯作者：
WEINGART, R
中科院分区：
文献类型：
--
作者：
KASS, RS;LEDERER, WJ;WEINGART, R
在Strophanthidin的影响下，浦肯野纤维[小牛心脏]表现出瞬间内向电流(TI)，这有助于心律失常的活动。通过电压钳实验研究了钙离子在这一现象中的作用。TI的幅度与细胞外钙浓度CaO成正比。镁离子具有拮抗作用。心动过速与心力阶段性增加(后收缩)密切相关。像TI一样，后收缩是由前一个动作电位或强去极化脉冲的中断引起的。虽然峰力电流先于峰力电流50-100ms，但TI和后收缩表现出相似的波形。通过增加前一个去极化脉冲的强度或持续时间来增强这两个瞬变。随着脉冲后的电势水平向负方向移动，这两个事件都被减缓了。在没有强心激素的情况下，可通过强烈升高CaO而诱发TI和后收缩。对TI反映钙离子内流的假设进行了研究。Mn对TI有抑制作用，但抑制作用的发展和消除远远滞后于慢内向电流的作用。可以通过在正方向上改变膜电位来抑制并最终反转TI。反转电位平均为-5 mV，与钙通道不一致。后收缩与电流的相位电导变化的关系比与电流本身的关系更密切。细胞内钙的振荡释放显然是后收缩和产生TI的电导变化的主要事件。洋地黄中毒或非常高的CaO可能通过升高细胞内钙水平促进这种事件的发生。
Under the influence of strophanthidin, Purkinje fibers [calf heart] exhibit transient inward current (TI) which contributes to arrhythmogenic activity. Voltage-clamp experiments were carried out to study the role of Ca ions in this phenomenon. The amplitude of TI varied directly with the extracellular Ca concentration, Cao. Mg ions had an antagonistic effect. TI was closely associated with a phasic increase in force (aftercontraction). Like TI, the aftercontraction was evoked by a preceding action potential or by the break of a strong depolarizing pulse. TI and the aftercontraction displayed similar wave forms although peak force current preceded peak force by 50-100 ms. Both transients were enhanced by increasing the strength or duration of the preceding depolarization pulse. Both events were slowed as the potential level following the pulse was displaced in the negative direction. TI and the aftercontraction may be evoked in the absence of cardiotonic steroids by strongly elevating Cao. The hypothesis that TI reflects an influx of Ca2+ ions was studied. Mn inhibited TI but the development and removal of the inhibition lagged far behind the effects on the slow inward current. TI may be suppressed and eventually inverted by varying the membrane potential in the positive direction. The inversion potential averaged -5 mV and was not consistent with a Ca-specific pathway. The aftercontraction was more closely related to the phasic conductance change underlying the current than to the current flow itself. An oscillatory release of Ca from an intracellular store apparently is the primary event underlying the aftercontraction and the conductance change which generates TI. Digitalis intoxication or very high Cao may promote such events by elevating intracellular Ca levels.