Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of Glucagon on 35 cholangiographic studies was examined. Relief of spasm at the choledochoduodenal sphincter resulted in consistently improved demonstration of this area. Diminished spasm-induced pain was also recorded. The use of intravenous Glucagon is recommended for cholangiographic studies where there is total biliary obstruction, or where there is unsatisfactory demonstration of the choledocho-duodenal area.
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PMID:Glucagon as a hypotonic agent in cholangiography. 42 23

Surgical management of extrahepatic cholestasis is frequently complicated by sepsis, which can be explained in part by diminished function of the reticuloendothelial system. We have explored the possibility that the metabolic response to infection may also be abnormal. Fischer 344 rats underwent either bile duct ligation (BDL) or sham operation and were studied 3 days after operation. Hepatic amino acid uptake measured in vivo by the accumulation of 14C-alpha-aminoisobutyric acid or in vitro by the rate of transport of 14C-alanine by isolated hepatocytes was unaltered in the BDL animals, while gluconeogenesis from alanine by viable hepatocytes from BDL rats was actually enhanced. However, the expected increase in hepatic amino acid uptake in response to endotoxin was diminished in the BDL animals. In addition, we observed impaired responses of the jaundiced animals to glucagon and interleukin-1, two mediators of the hepatic acute phase response to endotoxin. These data suggest that while hepatic amino acid transport is normal in the basal state, the rat with extrahepatic biliary obstruction does not respond appropriately to stress and that this defect cannot be explained solely on the basis of altered handling of endotoxin by the reticuloendothelial system.
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PMID:Impaired metabolic response to endotoxin in obstructive jaundice. 352 8

The renal vasodilator properties of six endogenous substances were tested before and 4 hr after ligation of the common bile duct. Two substances, acetylcholine and a glucocorticoid, retained their vasodilator properties at a fixed dose following acute biliary obstruction. Dopamine was still able to increase glomerular filtration rate and renal blood flow, but demonstrated an attenuated response. Several other agents, glucagon, glycine, and bradykinin, lost their renal vasodilator actions at the dosages employed. For these latter three compounds, control studies using sham-obstructed dogs and identical waiting periods demonstrated no loss of vasoactive effect. When the order of experimental protocol was reversed, i.e., acute biliary obstruction followed by a 4-hr period without obstruction, the same phenomenon was observed. When dogs were tested 5 days following biliary obstruction, glycine, glucagon, dopamine, and dexamethasone all failed to raise either GFR or renal perfusion. The infusion of bile or dialyzed bile, but not bile salts or bilirubin, also caused the failure of glucagon, glycine, and bradykinin to exert a renal vasoactive effect. Dogs with 4 hr of biliary obstruction appeared to react normally to the pressor effects of noradrenaline and angiotensin II and to the diuretic effects of iv furosemide. The obstruction of the bile ducts with percolation of bile constituents into the circulation appears to alter the sensitivity of the renal vasculature to certain endogenous vasoactive agents.
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PMID:Action of renal vasodilators in dogs following acute biliary obstruction. 669 81

Experimentally, biliary obstruction can produce morphological and functional changes in the pancreatic gland, whereas pancreatic obstruction may have short-term (hyperamylasemia, pancreatic edema, and lysosomal hydrolase redistribution) or long-term (acinar cell atrophy and interstitial fibrosis) effects. We created a pancreaticobiliary duct obstruction in rats to evaluate (a) exocrine and endocrine anatomobiochemical pancreatic modifications; (b) structural and functional liver alterations; and (c) the relationship, if any, between the alterations found in the two organs. Forty-five male Sprague-Dawley rats were subdivided on the basis of period of obstruction (from 1 to 28 days). In each rat serum we evaluated amylase, cholestatic and cytolytic indices, and glucose. In frozen pancreatic samples we measured insulin, glucagon, and DNA; in the liver the DNA content was determined. Histologically, ductal dilation and proliferation were evaluated for the liver, zymogen granules, and Langerhans' islets, and atrophy for the pancreas. Fibrosis was evaluated for both the liver and the pancreas. Short-term common pancreaticobiliary duct ligation caused an increase in serum amylase levels and mild pancreatic edema. Longer-term obstruction had either similar or different effects on the two organs. In the pancreas it caused fibrosis and exocrine and endocrine atrophy, but not acute pancreatitis. In the liver the main phenomena observed were fibrosis, ductal dilation, and proliferation.
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PMID:Effects of pancreaticobiliary duct obstruction on the exocrine and endocrine rat pancreas. 853 59

Inspissated bile syndrome (IBS) is a rare neonatal disease. In the majority of cases, it resolves spontaneously and treatment is conservative. Follow-up is recommended with close monitoring of laboratory tests. When IBS does not resolve spontaneously, a catheter can be inserted into the gallbladder for cholangiography, which allows irrigation and drainage. Despite this treatment, some biliary tract obstruction may persist. We report on the case of a 3-month-old infant whose continuous biliary obstruction caused by IBS was successfully managed by interventional radiology with the association of N-acetylcysteine and glucagon. Even as first-line agents, these would allow more rapid clearance of gallstones and prevent infectious complications of indwelling catheters as well as decrease the need for surgery.
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PMID:Association of N-acetylcysteine and glucagon during percutaneous cholangiography in the treatment of inspissated bile syndrome. 2561 75