镁离子在洋地黄中毒性心律失常中的治疗机制及强心苷在镁缺乏中的作用

On the therapeutic mechanism of Mg2+ in digitoxic arrhythmias and the role of cardiac glycosides in Mg depletion.

作者信息

Moe B H

出版信息

Magnesium. 1984;3(1):8-20.

Abstract

In 9 (of 17 attempted) experiments (8 aborted due to premature tissue death), transmembrane electrical activity was recorded from canine false tendons superfused with Mg-free Tyrode's solution to simulate hypomagnesemia. Oscillatory after-potentials (OAP) developed similar to those seen after exposure to 2 X 10(-7) M ouabain, a short-lasting (0.5-1 time the duration of an action potential) OAP that often reached threshold superimposed on a long-lasting (3-4 times as long as the short) OAP. Both forms of OAP were shown to be Ca2+-dependent, as both were prevented by 10(-7) M nifedipine, but only the short OAP were abolished by nifedipine once they had appeared, while high (5 mM = 10 times normal) Mg2+ both prevented and terminated short and long OAP in digitoxic preparations. Results suggest that cardiac glycosides may deplete Mg from the myocardium. The mechanism of the therapeutic action of Mg2+ in digitalis intoxication is discussed in light of its involvement in Ca2+ sequestration by the sarcoplasmic reticulum.

摘要

在17次尝试的实验中有9次（8次因组织过早死亡而中止），从用无镁台氏液灌注的犬类假腱中记录跨膜电活动，以模拟低镁血症。振荡后电位（OAP）的产生与暴露于2×10⁻⁷ M哇巴因后所见的相似，一种短暂的（动作电位持续时间的0.5 - 1倍）OAP，其常达到阈值并叠加在一个持久的（是短暂OAP的3 - 4倍长）OAP上。两种形式的OAP均显示为Ca²⁺依赖性，因为二者均被10⁻⁷ M硝苯地平所阻断，但只有短暂的OAP一旦出现就会被硝苯地平消除，而高浓度（5 mM = 正常浓度的10倍）的Mg²⁺在洋地黄中毒制剂中既能预防又能终止短暂和持久的OAP。结果表明强心苷可能会使心肌中的镁耗竭。根据镁参与肌浆网对Ca²⁺的螯合作用，讨论了Mg²⁺在洋地黄中毒治疗作用中的机制。