Studies in the nervous control of carbohydrate metabolism. I.—The position of the centre

Abstract

I. Puncture of the floor of the 4th ventricle of the brain in rabbits having an average amount of glycogen in the liver and muscles has no effect on the blood sugar level while the animals are under the anesthetic influence of luminal or amytal. Under similar conditions of anesthesia, injection of adrenaline results in hyperglycemia, but mechanical asphyxia or ether is without effect on the blood sugar level, and lesions of the brain, such as decerebration or injury in the region of the hypothalamus, only occasionally cause it to rise. When decerebration is performed in rabbits during the short period of anesthesia induced by the intraven. injection of amytal, marked hyperglycemia supervenes within 2 hrs., provided that the pons is involved. Decerebration anterior or posterior to this region seldom has any effect on the blood sugar level, except when it involves a narrow portion of the medulla adjacent to the pons.[long dash]II. Decerebration at the pons in rabbits, besides causing hyperglycemia has the following effects: (a) increases the % of lactic acid in the blood; (b) decreases the % of glycogen in the liver when this is above about 0.7 to start with, but usually increases it when below this level; (c) decreases the % of glycogen in the leg muscles. These changes are usually insignificant when decerebration is performed at other levels than the pons. When decerebration is at the medulla oblongata the muscle glycogen usually increases in %. The degree of hyperglycemia after decerebration bears no relationship to the initial % of glycogen in the liver and the muscles. The total amount of sugar which can be calculated as arising from the changes in the % of glycogen in the liver and the muscles during the course of a decerebration expt. in animals with low initial % of glycogen falls far short of that necessary to induce, by intraven. injection of glucose into a normal rabbit, a degree of hyperglycemia comparable to that actually observed. It is concluded that a process of gluconeogene-sis must be responsible for most of the extra sugar which appears in the blood after pontine decerebration. In animals with high initial % of glycogen in the liver and the muscles, most of the extra sugar may come from this source. The % of N.P.N. of the blood was not found to be significantly increased after pontine decerebration. The R. Q. is not affected by decerebration at the pons and the consumption of O2 may either increase or decrease somewhat. In one exp. the increase in O2 consumption was pronounced. Injection of glucose soln. into animals decerebrated at the pons has no effect on the fall in the % of glycogen in the leg muscles, but may retard the decline in that of the liver, or cause it to increase.[long dash]III. In rabbits in which there are small amounts of glycogen in the liver and muscles decerebration at the pons does not cause hyperglycemia under the following conditions: (a) double adrenalectomy, (b) atropine and section of both vagus nerves, (c) ergotam-ine and section of both vagus nerves, (d) amytal. In rabbits in which there are larger amounts of glycogen in the liver and muscles, as a result of recent feeding with carbohydrates, decerebration at the pons does cause hyperglycemia, under the above conditions, but it is usually not so pronounced. The influence of section of the hepatic nerves on decerebration hyperglycemia is uncertain, since this operation in itself is usually followed in the rabbit by an increase in the % of blood sugar. It is considered that when there is little glycogen in the liver decerebration hyperglycemia is due to stimulation of the gluconeogenic process in the liver by way of the parasympathetic nerves.