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缺氧、高钾血症和酸中毒对豚鼠心室肌膜动作电位和兴奋性的联合影响。

Combined effects of hypoxia, hyperkalemia and acidosis on membrane action potential and excitability of guinea-pig ventricular muscle.

作者信息

Kodama I, Wilde A, Janse M J, Durrer D, Yamada K

出版信息

J Mol Cell Cardiol. 1984 Mar;16(3):247-59. doi: 10.1016/s0022-2828(84)80591-x.

DOI:10.1016/s0022-2828(84)80591-x
PMID:6716491
Abstract

The effects of hypoxia (with and without acidosis) on membrane action potentials and recovery kinetics of their upstroke velocity (Vmax) were studied in isolated guinea-pig papillary muscles at various extracellular K+ concentrations. At 5 mM [K+]0, hypoxia (hypoxic and glucose-free perfusate) at pH 7.4 caused a progressive shortening of action potential duration and a slight decrease in Vmax and resting potential. The recovery kinetics of Vmax assessed by premature stimuli were not affected by hypoxia. At high [K+]0 of 10 or 12 mM, hypoxia caused a marked decrease in Vmax, while the shortening of the action potential and the decrease in resting potential were similar to those at 5 mM [K+]0. However, the recovery kinetics of Vmax were markedly slowed by hypoxia. When hypoxia was added in the presence of mild acidosis (pH 6.8), the shortening of the action potential due to hypoxia was appreciably less. However, other hypoxia-induced changes in action potential and in recovery kinetics of Vmax under normal and high [K+]0 were not influenced by the concomitant acidosis. These results show that the depressant effect of hypoxia on the action potential upstroke and on the recovery of excitability of ventricular myocardium is increased when the muscles are partly depolarized at high K+. Slight differences in extracellular K+ in the presence of hypoxia have a marked effect on the time course of recovery of excitability. This inhomogeneity in refractoriness could be important for the occurrence of re-entrant arrhythmias in ischemic myocardium.

摘要

在不同细胞外钾离子浓度下,研究了缺氧(伴有或不伴有酸中毒)对豚鼠离体乳头肌膜动作电位及其上升速度(Vmax)恢复动力学的影响。在[K⁺]₀为5 mM时,pH 7.4的缺氧(缺氧且无葡萄糖灌注液)导致动作电位持续时间逐渐缩短,Vmax和静息电位略有下降。通过过早刺激评估的Vmax恢复动力学不受缺氧影响。在[K⁺]₀为10或12 mM的高浓度时,缺氧导致Vmax显著下降,而动作电位缩短和静息电位下降与[K⁺]₀为5 mM时相似。然而,缺氧使Vmax的恢复动力学明显减慢。当在轻度酸中毒(pH 6.8)存在的情况下加入缺氧时,缺氧引起的动作电位缩短明显减少。然而,在正常和高[K⁺]₀条件下,其他缺氧引起的动作电位变化和Vmax恢复动力学不受伴随酸中毒的影响。这些结果表明,当肌肉在高钾状态下部分去极化时,缺氧对心室心肌动作电位上升支和兴奋性恢复的抑制作用增强。缺氧存在时细胞外钾离子的微小差异对兴奋性恢复的时间进程有显著影响。这种不应期的不均匀性可能对缺血心肌中折返性心律失常的发生很重要。

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