Insulin and glucagon response during hemorrhage induced hyperglycemia.
Rapid hemorrhage to 50 mmHg (1 mmHg = 133.322 Pa) in the pentobarbital-anesthetized cat leads to severe hyperglycemia which declines only slightly by 90 min of hemorrhage. Insulin levels decline to less than one-half of control levels and remain low throughout, despite the hyperglycemia. Glucagon levels decline at 15 min but are significantly elevated by 90 min. These data confirm that the hepatic glycogenolysis is controlled almost entirely by hepatic sympathetic nerves and adrenal secretions with no role for elevated glucagon levels at the early stages in hemorrhage. Hepatic denervation leads to lesser insulin suppression and greater glucagon elevation at later times (45 and 90 min), suggesting that intact hepatic nerves are required for a normal pancreatic response. Hepatic sympathectomy did not produce these effects. Insulin responses remained normal, but glucagon levels were suppressed throughout the entire experiment in sympathectomized cats. The data suggest that hepatic nerves may modulate insulin and glucagon levels during hemorrhage in an unknown manner.
D000315:Adrenalectomy; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology; D002415:Cats; D003714:Denervation; D004558:Electric Stimulation; D005934:Glucagon / Q000097:blood*; D006470:Hemorrhage / Q000097:blood*; D006943:Hyperglycemia / Q000097:blood* / Q000209:etiology; D007328:Insulin / Q000097:blood*; D008099:Liver / Q000294:innervation
D007328:Insulin; D005934:Glucagon