Inhibition of Hypoglycemic Perspiration by Spinal Anesthesia

Abstract

When the blood sugar falls to a critical level, many manifestations of sympathetic excitation present themselves in the so called hypoglycemic syndrome. The investigations of Cannon, McIver and Bliss 1 with the denervated heart, of Abe 2 with the denervated iris, of Houssay, Lewis and Molinelli 3 with their cross-circulation preparations, and others, 4 indicate that insulin hypoglycemia is associated with a discharge of epinephrine from the adrenal medulla. Inhibition of the sympathetic adrenal mechanism by any means (sympathectomy, splanchenectomy adrenal medulla ablation, ergotamine poisoning) prolongs the hypoglycemia. This indicates that epinephrine plays an important rôle in the regulation of and in compensation for any abnormal diminution of the blood sugar.

In man, we have no direct evidence that the phenomena observed during hypoglycemia are the result of excitation of the sympathetico-adrenal mechanism; our evidence is only inferred from the animal experimentation. During the course of studies on hypoglycemia experimentally produced in man, we observed that one of the earliest and prominent symptoms of a marked fall in the blood sugar, was profuse perspiration. The sweat glands receive nerve fibres which are entirely sympathetic in origin (Langley⁵). It is therefore not surprising that a mechanism apparently which excites the sympathetico-adrenal mechanism should produce profuse perspiration. That this is a “cause and effect” relationship can only be inferred. We could find no direct proof in the literature. To test the hypothesis we attempted to inhibit the sympathetic nervous system, employing spinal anesthesia for the purpose.