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Ischemia induced ventricular arrhythemias in the presence of hypokalemia

低钾血症时缺血诱发的室性心律失常

基本信息

批准号：
02670400
负责人：
YANO Katsusuke
金额：
$ 1.54万
依托单位：
Nagasaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1990
资助国家：
日本
起止时间：
1990 至 1992
项目状态：
已结题

项目摘要

During acute ischemia, myocardial cells release potassium ion that accumulate in the extracellular space because of reduced blood flow. The resulting altered potasslum gradients induce injury currents and are accompanied by typical electrophysiologic changes, which predispose the heart to ventricular arrhythmias. The present study was designed to examine changes in extracellular potassium during coronary occlusion and subsequent reperfusion, susceptibility of the heart to ventricular arrhythmias and electrophysiologic properties of the heart during myocardial ischemia in the dog with chronic hypopotassemia. To produce chronic hypopotassemia 20 dogs were fed special low-potassium diet and intramuscular administration (once a day) of furosemide (10 mg) and to produce normopotassmia 20 dog were fed ordinary diet for 4 weeks. Programmed ventricular stimulation was performed for induction of ventricular arrhythmias and for determination of effective refractory period and intraventricular conduction time. Extracellular potassium activity was recorded at normal and ischemic area of the heart during occlusion of the anterior descending coronary artery (LAD) and subsequent reperfusion. Extracellular potassium in the ischemic area of the heart was progressively increased during coronary occlusion and rapidly reduced after coronary reperfusion in the hypopotassemia and normopotassemia groups. The magnitude of increase in extracellular potassium was not significantly different between the two groups. Incidence of ventricular arrhythmias, dispersion of effective refractory period and intraventricular conduction delay in the ischemic area of the heart were greater in the dog with hypopotassemia than in the dog with normopotassemla. In conclusion, changes in extracellular potassium during coronary artery occlusion and subsequent reperfusion have important roles in the genesis of the ventricular arrhythmias in the presence of chronic hypopotassemia.

在急性缺血期间，由于血流减少，心肌细胞释放钾离子，钾离子积聚在细胞外间隙中。由此产生的改变钾梯度诱导损伤电流，并伴随着典型的电生理变化，使心脏易患室性心律失常。本研究旨在研究慢性低钾血症犬冠状动脉闭塞和随后再灌注期间细胞外钾的变化，心脏对室性心律失常的易感性以及心肌缺血期间心脏的电生理特性。用低钾饲料喂养20只狗，每日肌注速尿10 mg，造成慢性低钾血症;用普通饲料喂养20只狗，造成正常钾血症，共4周。进行程序心室刺激以诱导室性心律失常并测定有效不应期和心室内传导时间。在冠状动脉前降支（LAD）闭塞和随后的再灌注过程中，在心脏的正常和缺血区域记录细胞外钾活性。在低钾血症和正常钾血症组中，心肌缺血区的细胞外钾在冠状动脉闭塞期间进行性增加，并在冠状动脉再灌注后迅速减少。两组间细胞外钾增加的幅度无显著差异。低钾血症犬的室性心律失常发生率、有效不应期离散度和心脏缺血区的心室内传导延迟均高于钾血症正常犬。总之，在冠状动脉闭塞和随后的再灌注过程中，细胞外钾的变化有重要作用的发生室性心律失常的慢性低钾血症的存在。