title: The effect of synacthen on acute necrotizing pancreatitis in rats.
abstract: OBJECTIVE
  This study investigates the hypothesis that an adrenocorticotropic hormone-analog therapy may ameliorate relative adrenal insufficiency in the early phase of acute necrotizing pancreatitis (NP) by boosting endogenous glucocorticoid production.
  
  
  METHODS
  Forty Wistar rats with taurocholate-induced NP were divided into 5 groups: the first group received low-dose Synacthen (0.5 mg/kg); the second, high-dose Synacthen (5mg/kg); the third,low-dose cortisol (10 mg/kg); the fourth, high-dose cortisol (100 mg/kg); and the fifth, the control group, received no treatment. All animals were killed after 6 hours: concentrations of plasma corticosterone, interleukin 1 (IL-1), IL-6, IL-10, tumor necrosis factor alpha, amylase, and lipase in ascites, myeloperoxidase activity in the pancreas, and a histological score were evaluated.
  
  
  RESULTS
  Corticosterone increased neither in the low-dose nor in the high-dose Synacthen group. Synacthen did not improve the early course of NP in terms of laboratory and histological results. A reduction of pancreatic necrosis and inflammation was observed in the low-dose cortisol group.
  
  
  CONCLUSIONS
  Endogenous glucocorticoid release seemed to be at its maximum during the early stage of NP and could not be further increased by Synacthen. Low-dose exogenous cortisol ameliorated the disease. These findings support the existence of relative adrenal insufficiency in the early phase of acute NP.
authors.affiliation: Department of General Surgery, St Josef Hospital, Ruhr University, Bochum, Germany. c.mueller@klinikum-bochum.de
authors.forename: Christophe A
authors.initials: CA
authors.lastname: Muller
authors.forename: Nicholas
authors.initials: N
authors.lastname: McArthur
authors.forename: Orlin
authors.initials: O
authors.lastname: Belyaev
authors.forename: Wenzel
authors.initials: W
authors.lastname: Burr
authors.forename: Jens
authors.initials: J
authors.lastname: Werner
authors.forename: Andreas
authors.initials: A
authors.lastname: Meiser
authors.forename: Dirk
authors.initials: D
authors.lastname: Weyhe
authors.forename: Markus W
authors.initials: MW
authors.lastname: Büchler
authors.forename: Waldemar
authors.initials: W
authors.lastname: Uhl
mesh_terms: D000309:Adrenal Insufficiency / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D000681:Amylases / Q000378:metabolism; D000818:Animals; D003366:Cosyntropin / Q000494:pharmacology*; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D018450:Disease Progression; D005260:Female; D006854:Hydrocortisone / Q000097:blood / Q000494:pharmacology*; D008049:Lipase / Q000378:metabolism; D010179:Pancreas / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D019283:Pancreatitis, Acute Necrotizing / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013656:Taurocholic Acid; D013997:Time Factors
chemical_list: D016207:Cytokines; D003366:Cosyntropin; C006418:adrenocorticotropin zinc; D013656:Taurocholic Acid; D009195:Peroxidase; D008049:Lipase; D000681:Amylases; D006854:Hydrocortisone