Specter M J, Schweizer E, Goldman R H
Circulation. 1975 Dec;52(6):1001-5. doi: 10.1161/01.cir.52.6.1001.
The mechanism by which magnesium affects digitalis-induced arrhythmias was studied in dogs with and without beta-receptor blockade. Digoxin was infused at a rate of 2.5mug/kg/min until ventricular tachycardia developed, then half the animals were given MgSO4, the other half saline. In animals given MgSO4, sinus rhythm was immediately re-established; in animals given saline, ventricular tachycardia persisted. In animals with beta-receptor blockade, MgSO4 was as effective in abolishing ventricular tachycardia as in those without beta-receptor blockade. We found no evidence that magnesium re-activated digoxin-inhibited (Na+, K+)-ATPase, altered myocardial or microsomal digoxin binding, or acted via the autonomic nervous system. Magnesium's direct effect on calcium and potassium fluxes across the myocardial cell membrane may be the mechanism of its antiarrhythmic action in digitalis-toxic arrhythmias.
在有或没有β受体阻断的犬中研究了镁影响洋地黄所致心律失常的机制。以2.5μg/kg/分钟的速率输注地高辛，直至发生室性心动过速，然后将一半动物给予硫酸镁，另一半给予生理盐水。给予硫酸镁的动物，窦性心律立即恢复；给予生理盐水的动物，室性心动过速持续存在。在有β受体阻断的动物中，硫酸镁消除室性心动过速的效果与没有β受体阻断的动物相同。我们没有发现镁重新激活地高辛抑制的（钠，钾）-ATP酶、改变心肌或微粒体地高辛结合或通过自主神经系统起作用的证据。镁对心肌细胞膜钙和钾通量的直接作用可能是其在洋地黄中毒性心律失常中抗心律失常作用的机制。
