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低钾细胞外液对豚鼠心室肌细胞有效不应期临界电位的影响及其机制

Effects and mechanism of low [K]o on the critical potential of effective refractory period in guinea pig ventricular muscle cells.

作者信息

Li C, Zeng Y M, Zhuang C X, Liu T F

机构信息

Department of Physiology, Shantou University Medical College, PR China.

出版信息

Methods Find Exp Clin Pharmacol. 1992 Mar;14(2):107-13.

PMID:1598022
Abstract

1.5 mM KCl Tyrode's solution enabled the critical potential (-55-60 mV) of effective refractory period to shift in a positive direction in guinea pig ventricular muscle cells. In 1.5 mM KCl Tyrode's solution, the probability of testing AP's initial potential positive to -54 mV in the repolarizing phase was as high as 80% (n = 10), but the percentage in 4.5 mM [K]o group was only 11% (n = 35). The mean value of the positive shift was 30.2 +/- SD 17 mV. Testing APs had higher values of overshoots (mean = 23 +/- 13.8 mV); their mean Vmax was 98 V/s. Early after depolarization and positive inotropic effects appeared. 13.5 mM KCl, in contrast to 1.5 mM KCl, produced contrary effects. Phenomena indicated that early after depolarization in low [K]o was associated with the positive shift of critical potential of effective refractory period. Above-mentioned effects of 1.5 mM KCl could not be completely eliminated by verapamil, but could be abolished by an inactivation promoting agent of sodium channel, lidocaine 7.4 x 10(-5) M (n = 10). The results suggest that accelerating recovery time and shifting recovery potential in the positive direction of inactivated sodium channel might be the principal reasons for the effects of low [K]o. The role of the Na+ pump inhibitor, ouabain, was not similar to that of 1.5 mM KCl Tyrode's solution except for positive inotropic effect.

摘要

1.5 mM氯化钾的台氏液可使豚鼠心室肌细胞有效不应期的临界电位(-55 - 60 mV)正向偏移。在1.5 mM氯化钾的台氏液中,复极化阶段动作电位(AP)初始电位正向超过 -54 mV的检测概率高达80%(n = 10),但在4.5 mM [K]o组中该百分比仅为11%(n = 35)。正向偏移的平均值为30.2 +/-标准差17 mV。检测到的动作电位有更高的超射值(平均值 = 23 +/- 13.8 mV);其平均最大上升速率为98 V/s。出现了早期后去极化和正性肌力作用。与1.5 mM氯化钾相比,13.5 mM氯化钾产生相反的作用。这些现象表明低[K]o时的早期后去极化与有效不应期临界电位的正向偏移有关。1.5 mM氯化钾的上述作用不能被维拉帕米完全消除,但可被钠通道失活促进剂7.4 x 10(-5) M的利多卡因消除(n = 10)。结果表明,加速失活钠通道的恢复时间并使其恢复电位正向偏移可能是低[K]o产生这些作用的主要原因。除正性肌力作用外,钠泵抑制剂哇巴因的作用与1.5 mM氯化钾台氏液的作用不同。

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