THE MECHANISM OF HYPERGLYCEMIA DURING ANESTHESIA

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Abstract
Hepatotoxic narcotics (ether and chloroform) produce marked hyperglycemia; non-hepatotoxic agents (N2O, pentothal and cyclopropane) produce minimal hyperglycemia if there is no hypoxia. Five rabbits of 1.5-2 kg. were given 15 min. of ether narcosis. Blood sugar rose to 200-250 mg.% and returned to normal (100-130 mg.%) in 2-3 hrs. With 1 hr. of ether anesthesia, the blood sugar rose to 300 mg.% and returned to normal in 3-4 hrs.; N2O-induced hypoxemia caused a rise to 200 mg.%. In rabbits subjected to a 2-stage bilateral adrenalecto-my, 15 min. of ether narcosis, or N2O-induced hypoxemia produced no hyperglycemia. Ether anesthesia was repeated on rabbits under high pontocaine spinal anesthesia (T4); if hypotension (hypoxemia) was prevented, no hyperglycemia developed. However, rabbits under spinal anesthesia to T6 reacted with hyperglycemia to ether narcosis because the adrenal glands were not denervated. It seems that ether produces a central stimulation transmitted to the adrenals via the sympathetics, whence hyperadrenalinemia induces hepatic glycogenolysis. .Clinically, high spinal anesthesia is useful in avoiding hyperglycemia.

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