A DELIMITATION OF THE CENTRAL NERVOUS MECHANISM INVOLVED IN REFLEX HYPERGLYCEMIA

Abstract

Reflex rises in the blood sugar of cats, induced before and after exclusion of various parts of the central nervous system, were compared to ascertain whether or not a bulbar control of carbohydrate mobilization exists. Intact, decerebrate and thalamic animals anesthetized with Na barbital and chloralose showed reflex rises ranging roughly from 20 to 40 mgm. %. Stimulation of an afferent nerve had little or no effect on the blood sugar levels of 15 decapitate animals. In 10 experiments a diagonal section through the medulla oblongata from a point 1 or 2 mm. rostral to the union of the cerebellum and brachium pontis dorsally to the posterior border of the pons ventrally did not abolish reflex hyperglycemia, for the average reflex rise was 22 mgm. % in 6 under intravenous Na barbital and 32 mgm. % in 4 under chloralose. But a section a few mm. caudal to that level abolished the phenomenon almost entirely (4 cases), causing the animals to react like decapitate preparations. The author concludes that there is in the floor of the 4th ventricle just posterior to the middle of the brachium pontis and very close to the vasomotor center a neural mechanism responsible for the reflex rises in blood sugar which result when an afferent nerve is stimulated in the anesthetized cat.