Control hof the hyperglycemic response to hemorrhage in cats

Abstract

Rapid hemorrhage to 50 mmHg (1 mmHg = 133.322 Pa) mean arterial blood pressure led to a rise in blood glucose levels that reached a level of 500 mg% by 15 min and was then maintained with minor decreases for the full period of hemorrhage (90 min). From changes in hepatic glycogen levels it is estimated that glucose from 3.1 g of glycogen was released per kilogram of body weight over the 90-min period of hemorrhage. Bilateral adrenalectomy or hepatic denervation did not reduce the hyperglycemic response significantly although adrenalectomy tended to produce a lesser response. Removal of the adrenals and the hepatic nerves (surgically or selective hepatic sympathectomy using 6-hydroxydopamine) eliminated all but a very small hyperglycemic response which was of slow onset. Thus, the hyperglycemic response to hemorrhage is controlled by a redundant control system wherein either the adrenals or the hepatic sympathetic nerves can produce the response but elimination of both systems eliminates the response. The minor hyperglycemia that occurred with both systems eliminated shows that other hormonal changes known to occur during hemorrhage play, at most, a minor role in the direct stimulation of glycogenosis during hemorrhage.