Lai Zhong-fang
Department of Pharmacology, School of Medicine, Kumamoto University, Kumamoto 860-0811, Japan.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2002 Apr;24(2):190-6.
We investigated the effects of simulated ischemia on intracellular Cl- concentration ([Cl-]i) in guinea pig ventricular myocardial cells and possible role of the [Cl-]i on the ischemia/reperfusion-induced arrhythmias in perfused rat hearts. Our results provided direct evidence that the [Cl-]i in ventricular muscle was increased under ischemic conditions, which suggested that activation of the Cl-(-)HCO3- exchanger by ischemia would partially contribute to the elevation of [Cl-]i. Application of stilbene derivatives or lowering Cl- concentration in perfusion solution delayed the onset of ischemia-induced deterioration in action potentials, pHi, [Cl-]i, and suppressed the incidence of ischemia/reperfusion-induced arrhythmias. The conclusion was made to emphasize the important role of intracellular Cl- homeostasis in cardiac physiology and pathogenesis of myocardial ischemia/reperfusion injury.
我们研究了模拟缺血对豚鼠心室肌细胞内氯离子浓度（[Cl-]i）的影响，以及[Cl-]i在灌注大鼠心脏缺血/再灌注诱导心律失常中的可能作用。我们的结果提供了直接证据，表明缺血条件下心室肌中的[Cl-]i升高，这表明缺血激活Cl-(-)HCO3-交换体将部分导致[Cl-]i升高。应用芪衍生物或降低灌注液中的氯离子浓度可延迟缺血诱导的动作电位、细胞内pH值、[Cl-]i恶化的发生，并抑制缺血/再灌注诱导心律失常的发生率。得出的结论是强调细胞内氯离子稳态在心脏生理和心肌缺血/再灌注损伤发病机制中的重要作用。
