[K+]o accumulation and electrophysiological alterations during early myocardial ischemia.
[K+]o accumulation and electrophysiological alterations during early myocardial ischemia.
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早期心肌缺血期间[K]o 的积累和电生理变化。
DOI：
10.1152/ajpheart.1982.243.2.h318
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Shine,KI
中科院分区：
文献类型：
--
作者：
Weiss,J;Shine,KI
采用双管呋喃霉素K+敏感电极和漂浮微电极分别监测全脑缺血无侧支循环和缺氧维持血流状态下，离体兔动脉灌注室间隔细胞外K+浓度([K+]o)和细胞内电位。在缺血时，[K+]o以0.5-1 mm/min的速率重复性升高，通常呈三相模式，并伴有动作电位时程缩短和传导时间延长。等同于缺血时的高钾血症和呼吸性酸中毒(pH 6.2-6.5)和儿茶酚胺可定量复制缺血引起的时程和CT的改变。这些因素都不能单独产生数量上可比的电生理变化。较快的心率增加了缺血期[K+]o的积聚，并加剧了缺血期时程和CT的变化。这些发现提示缺血早期局部高血钾、细胞内酸中毒和儿茶酚胺释放可能是导致折返性心律失常发生的电生理改变的原因。
Double-barreled valinomycin K+-sensitive electrodes and floating microelectrodes were used to monitor extracellular K+ concentration ([K+]o) and intracellular potential, respectively, in the isolated arterially perfused rabbit interventricular septum, under conditions of global ischemia without collateral flow and hypoxia with maintained flow. During ischemia [K+]o reproducibly increased at rates of 0.5-1 mM/min, usually in a triphasic pattern, and was accompanied by shortening of the action potential duration (APD) and an increase in conduction time (CT). Hyperkalemia, equivalent to that occurring during ischemia, in combination with respiratory acidosis (pH 6.2-6.5) and catecholamines reproduced quantitatively the ischemia-induced changes in APD and CT. None of these factors alone produced quantitatively comparable electrophysiological changes. Faster heart rates increased [K+]o accumulation during ischemia and accentuated the changes in APD and CT during ischemia. These findings suggest that local hyperkalemia, intracellular acidosis, and catecholamines release during early ischemia may account for electrophysiological changes predisposing to the development of reentrant arrhythmias.