Early endoscopic sphincterotomy in patients with gallstone pancreatitis.
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Biomedical subjects
Publications and source records attributed to R M Ludewig.
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Glucagon can depress normal animal and human pancreatic exocrine secretions and modify experimentally-induced pancreatitis in animals. It has yet to be demonstrated that glucagon has any efficacy in the treatment of the diseased pancreas in man. Glucagon might act on the exocrine pancreas by 1. reducing pancreatic blood flow, 2. decreasing gastric secretion, 3. lowering serum calcium levels by the release of calcitonin, 4. acting to inhibit the secretin mechanism, 5. causing a hyperglycemia and 6. degranulating pancreatic acinar cells. While a reduction in pancreatic blood flow, an inhibition of the secretin mechanism and a hyperglycemia seemed to have been ruled out as possible mechanisms of action, there is too little available data to effectively speculate on the mechanism(s) of action of glucagon on the exocrine pancreas.
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Acute hemorrhagic pancreatitis was created in dogs using the closed duodenal loop technique. After 18 hours, a a constant rate of pancreatic exocrine secretion was stimulated with secretin. A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered to dogs with acute hemorrhagic pancreatitis. The acute hemorrhagic pancreatitis reduced the sensitivity of the exocrine pancreas to secretin and antidiuretic hormone.
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