Mugelli A, Cerbai E, Barbieri M, Li Q
Department of Pharmacology, University of Firenze, Italy.
Pharmacol Res. 1995 Mar-Apr;31(3-4):243-9. doi: 10.1016/1043-6618(95)80025-5.
Oxygen radicals (OR) generated at the time of reflow of the ischaemic myocardium may cause 'reperfusion injury'. To protect myocardium from this injury, it is important to understand how OR cause their deleterious effects on myocytes. Here we describe the basic electrophysiological alterations caused by OR in patch-clamped ventricular myocytes isolated from the rat heart. Oxygen radicals generated by dihydroxyfumarate (DHF) caused a lengthening of action potential duration (APD) and the appearance of arrhythmogenic alterations such as early and delayed afterdepolarizations. Prolongation of APD was accompanied by a reduction in calcium and potassium currents. When intracellular calcium levels were kept constantly low by 500 microM EGTA in the pipette solution, the effects of DHF on action potential duration and the occurrence of early afterdepolarizations were largely prevented. It is concluded that exposure to OR may induce electrophysiological alterations in isolated myocytes. They are related to changes in specific ionic currents and in levels of intracellular calcium.
缺血心肌再灌注时产生的氧自由基（OR）可能会导致“再灌注损伤”。为了保护心肌免受这种损伤，了解OR如何对心肌细胞产生有害影响非常重要。在此，我们描述了从大鼠心脏分离的膜片钳记录的心室肌细胞中OR引起的基本电生理改变。二羟基富马酸（DHF）产生的氧自由基导致动作电位时程（APD）延长，并出现诸如早期和延迟后去极化等致心律失常改变。APD延长伴随着钙电流和钾电流的减少。当通过移液管溶液中的500微摩尔乙二醇双四乙酸（EGTA）使细胞内钙水平持续保持较低时，DHF对动作电位时程和早期后去极化发生的影响在很大程度上得到了预防。得出的结论是，暴露于OR可能会在分离的心肌细胞中诱导电生理改变。它们与特定离子电流的变化以及细胞内钙水平有关。
