Abstract | BACKGROUND: AIMS: 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). CONCLUSION:
|
Authors | J W Chen, A Thomas, C M Woods, A C Schloithe, J Toouli, G T Saccone |
Journal | Gut
(Gut)
Vol. 47
Issue 4
Pg. 539-45
(Oct 2000)
ISSN: 0017-5749 [Print] England |
PMID | 10986215
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
|
Chemical References |
- Carbachol
- Amylases
- Sincalide
|
Topics |
- Acute Disease
- Amylases
(blood)
- Animals
- Carbachol
- Female
- Ligation
- Male
- Opossums
- Pancreatitis
(blood, etiology)
- Sincalide
- Spasm
(blood, complications)
- Sphincter of Oddi
(drug effects, physiopathology)
|