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。     

A Reevaluation of the Critical Membrane Potential of the Effective Refractory Period in Guinea Pig Ventricular Fibres

The traditional critical membrane potential (CMP), -55—-60mV, which corresponds to effective refractory period (ERP), was anew investigated in guinea pig ventricular muscle fibres. The electrical and contractile responses to the stimulus during repolarization of action potential (AP), particularly from+10 to -60 mV, were observed. One third of 35 tested cells displayed testing action potential (TAP) and local response at≥-54 mV when they were stimulated by testing pulses in 37℃ normal Tyrode's solution. Potential level of TAP which occurred earliest was at -30 mV and that of local response which appeared earliest was at 0 mV during repolarization among 95 systematic tests. Most of the TAPs belonged to the slow response potential type. The ratio of TAP evoked at ≥-54 mV initial membrane potential (IMP) was as high as 86% when the experiment was carried out in 37℃ 1.5 mmol KC1/L Tyrode's solution. In view of distribution of IMPs of TAPs, the CMP of ERP in guinea pig ventricular muscle fibres was more     

Characteristics of Early Afterdepolarization in Mouse Atrial Fibers

Early afterdepolarization (EAD) in mouse atrial fibers was investigated under the treatment with aconitine, 3. 0 mmol/L K+ ,quinidine, ryanodine or Bay k 8644. All of these EADs possessed the following common characteristics j all the parameters of EAD showed cycle length-dependence; take-off potential of the first triggered burst played an important role in the generation of the other parameters ; hyper-polarization of the triggered brust enhanced the end of EAD; and the second plateau response might be used as an indicator of the capability of EAD generation of myocardiac cell. All those EADs were inhibited or abolished by nifedipine, tetrodotoxin or lidocaine. Potassium channel activators, lemakalim, thalium ion, acetyl-choline or high potassium could also inhibit or abolish the EADs. It is suggested that the EADs induced by different agents may base on a common mechanism ; all currents contributing to the plateau phase of the action potential play an important role in the generation of EAD.     

在豚鼠心室肌重新探讨有效不应期的临界膜电位值

本文在豚鼠心室肌重新探讨心肌有效不应期(ERP)的传统临界膜电位值(CMP)(-55—160mV),观察细胞动作电位(AP)复极到+10—-60mV时,对试验刺激的电反应和收缩反应。37℃正常台氏液中,中等强度的试验刺激下,35个细胞中,约有1/3的细胞,在正于-54mV出现局部反应和试验AP。最高在0mV开始出现局部电位,-30mV开始出现试验AP,多数属慢反应电位。37℃ 1.5mmol/L KCl台氏液中,在正于-54mV引发试验AP的比率高达86％。从试验AP的起始膜电位的分布,说明豚鼠心室肌ERP的CMP,正于Hoffman等确定的传统临界值,有相当范围可变性。每个心室肌纤维的临界值也不相同,接近正态分布。ERP与相对不应期界线并不严格。较高温度和低[K]_0是使ERP的CMP正移的主要因素。     

小鼠心房肌早发后去极化的特性

在小鼠心房肌上观察了由乌头碱、3.0mmol/L K~+、奎尼丁、ryanodine及Bay k8644引起的早发后去极化(EAD)。这些EAD具有以下共同特性:EAD的诸参数均呈周长依赖性;其中第一个触发发放的起步电位对其他参数起决定性作用;触发发放的后超极化促进EAD结束;第二平台反应是心肌细胞产生EAD能力的指标。上述所有EAD均可由硝苯吡啶、河豚毒素或利多卡因抑制或消除。钾通道激动剂:lemakalim,Ti~+,乙酰胆碱或高钾也可抑制或消除EAD。结果提示,由不同因素引起的EAD可能基于下列共同机制:参与动作电位平台期的各种电流均可在EAD形成中发生作用。