Boachie-Ansah G, Kane K A, Rankin A C
Department of Physiology & Pharmacology, University of Strathclyde, Glasgow, U.K.
J Cardiovasc Pharmacol. 1992 Oct;20(4):538-46. doi: 10.1097/00005344-199210000-00005.
The aim of this study was to determine the electrophysiological effects of a combination of factors that are of importance during myocardial ischaemia, i.e., acidosis, lactate, and lysophosphatidylcholine, in ventricular myocytes. Intracellular microelectrode techniques were used to record action potential and ionic currents in ventricular myocytes before, during, and after a 30 min exposure to a salt solution that was acidotic (pH 6.8), and contained lactate (10 mM) and lysophosphatidylcholine (5 microM). Single ventricular myocytes were dissociated enzymatically from guinea pig hearts, and perfused with either normal or modified physiological salt solution. Combined acidosis, lactate, and lysophosphatidylcholine resulted in a reduction in the resting membrane potential and maximum rate of depolarisation of phase 0, and flattening of the plateau but prolongation of the action potential duration at 90% repolarisation. Automatic activity was also induced in about one-third of the cells studied. Under voltage-clamp conditions, this combination of factors reduced the peak inward calcium current, on repolarisation after a depolarising step, reduced the steady-state outward current, and reduced the delayed rectifier current, measured as the tail current at the end of a depolarising clamp step. In some cells, a transient inward current was induced by the modified salt solution. It is concluded that the characteristic alterations in action potential characteristics induced by a combination of acidosis, lactate, and lysophosphatidylcholine are likely to result from reductions in the inward Ca current and the background and delayed rectifier K current.
本研究的目的是确定在心肌缺血期间具有重要意义的多种因素（即酸中毒、乳酸和溶血磷脂酰胆碱）组合对心室肌细胞的电生理影响。采用细胞内微电极技术记录心室肌细胞在暴露于酸性（pH 6.8）、含有乳酸（10 mM）和溶血磷脂酰胆碱（5 microM）的盐溶液30分钟之前、期间和之后的动作电位和离子电流。单个心室肌细胞通过酶解法从豚鼠心脏分离出来，并用正常或改良的生理盐溶液灌注。酸中毒、乳酸和溶血磷脂酰胆碱共同作用导致静息膜电位降低、0期最大去极化速率降低、平台期变平，但在90%复极化时动作电位持续时间延长。在所研究的细胞中约三分之一还诱导出了自动活动。在电压钳条件下，这种因素组合降低了去极化步骤后复极化时的内向钙电流峰值，降低了稳态外向电流，并降低了延迟整流电流（以去极化钳制步骤结束时的尾电流测量）。在一些细胞中，改良盐溶液诱导出了瞬时内向电流。结论是，酸中毒、乳酸和溶血磷脂酰胆碱组合诱导的动作电位特征的典型改变可能是由于内向钙电流以及背景电流和延迟整流钾电流降低所致。
