Grin J, Pellizzón O A, Raynald A
Cátedra de Farmacología, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Argentina.
Medicina (B Aires). 1996;56(3):231-40.
This paper reports an electrophysiological study on the antiarrhythmic and proarrhythmic actions of magnesium chloride and magnesium sulphate intravenous infusions. Magnesium kinetics in control dogs, following a pulse of magnesium chloride or magnesium sulphate, was not affected by the accompanying anion. The experiments were performed with mongrel dogs divided into three groups fed either a normal diet (group I), a low magnesium diet plus chlortalidone treatment and potassium supplementation (group IIA) or a low magnesium diet plus chlortalidone treatment and magnesium sulphate infusion (group II B). In group I, infusion of magnesium sulphate solution decreased plasma sodium, potassium and ventricular fibrillation threshold (VFT), prolonged the ventricular effective refractory period (VERP) and increased the urinary excretion of potassium. The infusion of magnesium chloride solution did not affect VFT, prolonged VERP, QTc, AH and PQ. In this group, sodium chloride or sulphate infusion did not affect the electrophysiological variables but sodium sulphate decreased plasma potassium levels. The group II A was characterized by the decreased levels of potassium and magnesium contents of plasma, lymphocytes and myocardium, decreased VERP and VFT and prolonged QTc. The intravenous infusion of magnesium sulphate solution depressed further VFT and plasma potassium and increased VERP. The acute infusion of potassium chloride solution increased plasma potassium and VFT. In group II B, plasma electrolyte levels and electrophysiological variables were not affected. We conclude that the clinically demonstrable, antiarrhythmic effect of magnesium infusion can be attributed to prolonged VERP. Magnesium sulphate infusion, however, produced potassium depletion and decreased VFT (a pro-arrhythmic effect). These adverse effects can be avoided infusing magnesium chloride solutions.
本文报道了一项关于静脉输注氯化镁和硫酸镁的抗心律失常及促心律失常作用的电生理研究。在对照犬中，静脉注射氯化镁或硫酸镁脉冲后，镁的动力学不受伴随阴离子的影响。实验选用杂种犬，分为三组，分别给予正常饮食（I组）、低镁饮食加氯噻酮治疗及补钾（IIA组）或低镁饮食加氯噻酮治疗及硫酸镁输注（IIB组）。在I组中，输注硫酸镁溶液可降低血浆钠、钾水平及心室颤动阈值（VFT），延长心室有效不应期（VERP），并增加尿钾排泄。输注氯化镁溶液对VFT无影响，但可延长VERP、QTc、AH及PQ间期。在该组中，输注氯化钠或硫酸钠对电生理变量无影响，但硫酸钠可降低血浆钾水平。IIA组的特点是血浆、淋巴细胞及心肌中的钾和镁含量降低，VERP和VFT降低，QTc延长。静脉输注硫酸镁溶液可进一步降低VFT和血浆钾水平，并增加VERP。急性输注氯化钾溶液可增加血浆钾水平和VFT。在IIB组中，血浆电解质水平和电生理变量未受影响。我们得出结论，临床上可证实的镁输注的抗心律失常作用可归因于VERP延长。然而，输注硫酸镁会导致钾缺乏并降低VFT（一种促心律失常作用）。输注氯化镁溶液可避免这些不良反应。
