K~+-FREE INDUCED EARLY AFTERDEPOL-ARIZATION IN CARDIAC VENTRICULAR FIBERS OF GUINEA PIG AFTER COLD TREATMENT

The genesis and elimination of early afterdepolarizations (EADs) have been investigated in guinea pig cardiac ventricular fibers after a short period of cooling (5h, 2—4℃). After rewarming them to 37℃, EADs could be induced by K~+-free superfusion at an appropriate driving stimulation (0.2 Hz) in all preparations. A high level plateau, which linearly increases its duration with time, appears ahead of EADs. The critical point of the plateau occurred steadily at the level of -47±4 mV. Two types of triggered activity, all of which are the rhythmic activities in low level of membrane potential (-50 to -60 mV), appear on the platcau. There is no significant change after overdriving. Agonists of the Na-K pump (K~+ and Tl~+) could stop the rhythmic activity immediately and turn the low level of membrane potential to high one. The results showed that high level plateau is the basis of genesis of EADs, and the activation of Na-K pump plays an important part in stopping triggered rhythms arising from EADs.     

低温处理后由无钾引起的豚鼠心室肌早发后去极化

本文在短期低温处理后(5h,2—4℃)的豚鼠心室肌标本上,探讨了早发后去极化(EAD)的发生。在适当地驱动刺激(0.2Hz)下,复温后的心室肌标本经无钾溶液灌流后均可诱发EAD产生。EAD出现之前,动作电位于复极3期首先形成一新的“低位平台”。此平台可随时间呈线性增长,其拐点恒定在动作电位复极至—47±4mV的膜电位水平。由EAD触发形成的非驱动反应呈两种电位形式,但均属低膜电位水平(—50——60 mV)的节律性活动。超速驱动无明显影响,钠泵激动剂(K~+及Tl~+)可有效而迅速地终止触发性节律活动,并使低膜电位转变为高膜电位。结果表明:“低位平台”是EAD形成的基础;钠泵的激动在消除EAD触发的节律活动中起重要作用。