Clarkson C W, Ten Eick R E
Circ Res. 1983 May;52(5):543-56. doi: 10.1161/01.res.52.5.543.
Lysophosphatidylcholine, a putative biochemical mediator of ischemia-induced arrhythmias, reduces the resting potential of ventricular muscle. To elucidate possible mechanisms of lysophosphatidylcholine-induced depolarization, we investigated the effects of lysophosphatidylcholine on the electrophysiological properties of cat ventricular muscle, using potassium ion-selective electrodes and conventional microelectrode, current-, and voltage-clamp techniques. Lysophosphatidylcholine (50 microM) decreased the sensitivity of the resting potential to changes in extracellular potassium concentration. Hyperpolarization of lysophosphatidylcholine-depolarized fibers by current-clamp methods failed to reveal two stable levels of resting potential. Depolarizing concentrations of lysophosphatidylcholine did not reduce the potassium equilibrium potential, as determined from the reversal potential of the time-dependent potassium current and measurements of intracellular potassium activity using potassium ion-selective electrodes. Lysophosphatidylcholine induced a depolarizing shift of the reversal potential for steady state current, and did not induce the formation of a negative slope region in the steady state current-voltage or background current-voltage relationships. Lysophosphatidylcholine induced an inward shift and linearization of the background current-voltage relationship negative to -30 mV, and the lysophosphatidylcholine-sensitive component of the background current was an inward rectifier with a reversal potential approximately equal to the potassium equilibrium potential. Lysophosphatidylcholine also reduced the amplitudes of the time-dependent potassium current, slow inward current, and the potassium accumulation and depletion currents. These results indicate that lysophosphatidylcholine-induced depolarization is due, in part, to reduced potassium conductance at voltages near the normal resting potential, and that lysophosphatidylcholine may act as a nonspecific depressant of membrane channels.
溶血磷脂酰胆碱是缺血诱导性心律失常的一种假定生化介质，可降低心室肌的静息电位。为阐明溶血磷脂酰胆碱诱导去极化的可能机制，我们使用钾离子选择性电极以及传统微电极、电流钳和电压钳技术，研究了溶血磷脂酰胆碱对猫心室肌电生理特性的影响。溶血磷脂酰胆碱（50微摩尔）降低了静息电位对细胞外钾浓度变化的敏感性。通过电流钳方法使溶血磷脂酰胆碱去极化的纤维发生超极化，未能揭示出两个稳定的静息电位水平。从时间依赖性钾电流的反转电位以及使用钾离子选择性电极测量细胞内钾活性所确定的结果来看，去极化浓度的溶血磷脂酰胆碱并未降低钾平衡电位。溶血磷脂酰胆碱诱导了稳态电流反转电位的去极化偏移，并且在稳态电流-电压或背景电流-电压关系中未诱导形成负斜率区域。溶血磷脂酰胆碱诱导了背景电流-电压关系在负至-30毫伏时向内偏移并线性化，并且背景电流的溶血磷脂酰胆碱敏感成分是一种内向整流器，其反转电位大约等于钾平衡电位。溶血磷脂酰胆碱还降低了时间依赖性钾电流、缓慢内向电流以及钾积累和消耗电流的幅度。这些结果表明，溶血磷脂酰胆碱诱导的去极化部分是由于在接近正常静息电位的电压下钾电导降低所致，并且溶血磷脂酰胆碱可能作为膜通道的非特异性抑制剂发挥作用。
