EFFECTS OF HYPOGLYCEMIA AND PENTOBARBITAL SODIUM ON ELECTRICAL ACTIVITY OF CEREBRAL CORTEX AND HYPOTHALAMUS (DOGS)

Abstract

Electrograms have been recorded from the dog cortex (18 dogs) and from anterior and posterior hypothalamus (14 dogs) both with and without anesthetic under varying conditions of insulin hypoglycemia. The effect of hypoglycemia on the cortical activity is similar to that in man, the a rhythms are slowed and the [DELTA] waves increase in prominence. In more prolonged hypoglycemia the cortical responses fail completely and are restored only an hr. or so after inj. of glucose. Both post. and ant. hypothalamus show much stability compared to the cortex. No changes are noted until some time after failure of electrical activity of the cortex when a short period of hyperactivity of the hypothalamic centers may develop, followed later by failure just before death. Injected glucose restores hypothalamic activity some time before that of the cortex. Nembutal, which reduces cortical respiration in vitro, produces cortical changes similar to those of hypoglycemia except that it considerably enhances the amplitude of a waves at the same time that it slows their rhythm. In contrast to this, no differences are seen in hypothalamic rhythms before and after nembutal anesthesia. Results show independence of responses from cortex, from a region near the supraoptic nucleus, and from the mammillary body region. The latter 2 grid leads are approximately 1 cm. apart. The ant. hypothalamic response, recorded directly by our method, gives records indistinguishable from those obtained by the Grinker technic in which a grid lead is embedded in the bone at the roof of the pharynx. Changes (as much as 16-fold) in hydrostatic pressure of the cerebrospinal fluid are per se, without effect on the cortical electrogram.