Department of Physiology and Pharmacology of the Rockefeller Institute for Medical Research.
J Exp Med. 1916 May 1;23(5):655-67. doi: 10.1084/jem.23.5.655.
The foregoing experiments establish firmly the following facts. Subcutaneous or intramuscular injections of sodium oxalate in subtoxic doses, when administered to an animal which received a subminimal dose of magnesium sulphate, produce profound anesthesia and paralysis of long duration, although the usual effects of sodium oxalate alone are of a stimulating character. This fact is, in general, in harmony with the results reported by Starkenstein who, however, seems to have used the combination of the two salts in one solution; namely, that of magnesium oxalate. The combined injections of subminimal doses of sodium oxalate and magnesium sulphate produce a strong reduction, or even, at times, a complete abolition of the conductivity of the motor nerve endings. An intravenous injection of calcium salts brings on a recovery from the profound and prolonged effects of the combined action of sodium oxalate and magnesium sulphate, which is as prompt as is observed in experiments in which effective doses of magnesium alone were given. This fact is the more noteworthy, since depressions of long duration produced by prolonged continuous injections of magnesium solutions alone do not respond very promptly and effectively to calcium injections. As will be recalled, the starting point for our investigation was the hypothesis that substances which are capable of precipitating calcium-a biological antagonist of magnesium-ought to be capable of increasing the depressive effect of magnesium. Our experiments proved that this assumption was correct. This would seem, therefore, to justify the interpretation that the augmenting action of sodium oxalate has its cause in the ability of the latter to precipitate calcium and thus increase within the body the amount of unantagonized magnesium. However, we wish to state expressly that this view is, for the present, still no more than a hypothesis and does not exclude other possible interpretations of our facts. As we pointed out it speaks against this hypothesis that oxalates do not produce phenomena of depression; the toxic symptoms produced by oxalates exhibit distinctly signs of increased and not of decreased irritability.
上述实验确立了以下事实。给接受亚最小剂量硫酸镁的动物皮下或肌肉注射草酸钠亚毒性剂量，会产生深度麻醉和长时间瘫痪，尽管草酸钠本身的通常作用具有刺激性。这一事实通常与 Starkenstein 报告的结果一致，然而，他似乎在一个溶液中使用了两种盐的组合；即草酸镁。亚最小剂量草酸钠和硫酸镁的联合注射会强烈降低，甚至有时完全消除运动神经末梢的传导性。静脉注射钙盐会使草酸钠和硫酸镁联合作用产生的深度和长时间影响得到恢复，这种恢复速度与单独给予有效剂量镁的实验中观察到的一样迅速。这一事实更为重要，因为单独长时间连续注射镁溶液产生的长时间抑郁对钙注射的反应并不非常迅速和有效。如前所述，我们研究的起点是这样一种假设，即能够沉淀钙的物质（镁的生物拮抗剂）应该能够增强镁的抑制作用。我们的实验证明了这一假设是正确的。因此，这似乎可以解释为，草酸钠的增强作用是由于其沉淀钙的能力，从而在体内增加未拮抗的镁的量。然而，我们希望明确表示，目前，这种观点仍然只是一种假设，并不排除对我们的事实的其他可能解释。正如我们所指出的，草酸盐不会产生抑郁现象，这与该假设相矛盾；草酸盐产生的毒性症状表现出明显的兴奋性增加而不是降低的迹象。
