title: Sphincter of Oddi dysfunction produces acute pancreatitis in the possum.
abstract: BACKGROUND
  Sphincter of Oddi dysfunction has been implicated as a cause of various forms of acute pancreatitis. However, there is no direct evidence to show that sphincter of Oddi dysfunction can cause obstruction of trans-sphincteric flow resulting in acute pancreatitis.
  
  
  OBJECTIVE
  To determine if induced sphincter of Oddi spasm can produce trans-sphincteric obstruction and, in combination with stimulated pancreatic secretion, induce acute pancreatitis.
  
  
  METHODS
  In anaesthetised possums, the pancreatic duct was ligated and pancreatic exocrine secretion stimulated by cholecystokinin octapeptide/secretin to induce acute pancreatitis. In separate animals, carbachol was applied topically to the sphincter of Oddi to cause transient sphincter obstruction. Sphincter of Oddi motility, trans-sphincteric flow, pancreatic duct pressure, pancreatic exocrine secretion, plasma amylase levels, and pancreatic tissue damage (histology score) were studied and compared with variables in ligation models.
  
  
  RESULTS
  Acute pancreatitis developed following stimulation of pancreatic exocrine secretion with peptides after pancreatic duct ligation (p<0.05). Neither pancreatic duct ligation nor stimulation of pancreatic exocrine secretion with cholecystokinin octapeptide/secretin alone resulted in acute pancreatitis. Topical carbachol stimulated sphincter of Oddi motility abolished trans-sphincteric flow, and increased pancreatic exocrine secretion (p<0.05) and pancreatic duct pressure to levels comparable with pancreatic duct ligation (p<0.001). Carbachol application (with or without combined peptide stimulation) elevated plasma amylase levels (p<0.01) and produced pancreatic tissue damage (p<0.05). Decompression of pancreatic duct ameliorated these effects (p<0.05).
  
  
  CONCLUSIONS
  Induced sphincter of Oddi dysfunction when coupled with stimulated pancreatic secretion causes acute pancreatitis. This may be an important pathophysiological mechanism causing various forms of acute pancreatitis.
authors.affiliation: Department of General and Digestive Surgery, Flinders Medical Centre, Flinders University of South Australia, Australia.
authors.forename: J W
authors.initials: JW
authors.lastname: Chen
authors.forename: A
authors.initials: A
authors.lastname: Thomas
authors.forename: C M
authors.initials: CM
authors.lastname: Woods
authors.forename: A C
authors.initials: AC
authors.lastname: Schloithe
authors.forename: J
authors.initials: J
authors.lastname: Toouli
authors.forename: G T
authors.initials: GT
authors.lastname: Saccone
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D002217:Carbachol; D005260:Female; D008026:Ligation; D008297:Male; D009893:Opossums; D010195:Pancreatitis / Q000097:blood / Q000209:etiology*; D012844:Sincalide; D013035:Spasm / Q000097:blood / Q000150:complications*; D009803:Sphincter of Oddi / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D002217:Carbachol; D000681:Amylases; D012844:Sincalide