Insulin induced hypoglycemia and tolbutamide administration accompanied by much smaller falls in blood glucose were associated with increased pancreatic vein IRG concentrations in laparotomized dogs under barbiturate anesthesia. Hyperglycemia may have diminished pancreatic IRG release. Changes in IRG levels in peripheral and jejunal veins during hypoglycemia were unremarkable. In dogs, pancreatectomy was associated with no change in IRG release into a jejunal vein. Very small doses of glucagon administered intraportally during hyperglycemia were effective in promoting IRI release.
It is concluded that a fall in blood glucose from the basal state is a stimulus, and hyperglycemia is an inhibitor, of pancreatic IRG release. It is possible that glucagon may act in the basal state to deliver repeated small pulses of glucose and insulin into the circulation.