Role of glucagon in hyperglycemic response during a short period of hemorrhage in anesthetized dogs.

A role of pancreatic glucagon in hemorrhage induced hyperglycemia was studied in anesthetized dogs with or without functional adrenalectomy (ADRX), surgical hepatic denervation (HNX), and surgical pancreatectomy (PCX). Plasma epinephrine, norepinephrine, and glucose concentrations were determined in both hepatic venous and aortic blood. Plasma glucagon (IRG) and insulin (IRI) levels were determined in aortic blood. All dogs were bled until aortic systolic pressure dropped to approximately 50% (64.8 +/- 1.6 mmHg, n = 25) of its control value (136.7 +/- 4.4 mmHg, n = 25), and the hypotension was maintained for 5 min. In control dogs (n = 10), hemorrhage markedly increased aortic epinephrine and hepatic venous norepinephrine. Similarly, aortic IRG, hepatic venous glucose and aortic glucose rose significantly during hemorrhage. In dogs with HNX combined with ADRX (n = 10), aortic epinephrine and hepatic venous norepinephrine remained unchanged during hemorrhage. Aortic IRG concentration, however, increased to a level similar to that observed in the control group. Aortic glucose increased significantly along with significant increases in hepatic venous glucose. In dogs with PCX combined with HNX and ADRX (n = 5), the increases in aortic IRG, hepatic venous glucose and aortic glucose observed in the first two groups in response to hemorrhage were virtually abolished. The results indicate that the increase in aortic IRG during hemorrhage is of pancreatic origin. We conclude that the pancreatic glucagon may be involved in the hyperglycemic response to hemorrhage, most likely through glucose mobilization by the liver during the early phase of hemorrhagic hypotension.