Sphincter of Oddi dysfunction produces acute pancreatitis in the possum

Citation
Jwc. Chen et al., Sphincter of Oddi dysfunction produces acute pancreatitis in the possum, GUT, 47(4), 2000, pp. 539-545
Citations number
25
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
GUT
ISSN journal
00175749 → ACNP
Volume
47
Issue
4
Year of publication
2000
Pages
539 - 545
Database
ISI
SICI code
0017-5749(200010)47:4<539:SOODPA>2.0.ZU;2-T
Abstract
Background-Sphincter of Oddi dysfunction has been implicated as a cause of various forms of acute pancreatitis. However, there is no direct evidence t o show that sphincter of Oddi dysfunction can cause obstruction of trans-sp hincteric flow resulting in acute pancreatitis. Aims-To determine if induced sphincter of Oddi spasm can produce transsphin cteric obstruction and, in combination with stimulated pancreatic secretion , induce acute pancreatitis. Methods-In anaesthetised possums, the pancreatic duct was ligated and pancr eatic exocrine secretion stimulated by cholecystokinin octapeptide/secretin to induce acute pancreatitis. In separate animals, carbachol was applied t opically to the sphincter of Oddi to cause transient sphincter obstruction. Sphincter of Oddi motility, trans-sphincteric flow, pancreatic duct pressu re, pancreatic exocrine secretion. plasma amylase levels, and pancreatic ti ssue damage (histology score) were studied and compared with variables in l igation models. Results-Acute pancreatitis developed following stimulation of pancreatic ex ocrine secretion with peptides after pancreatic duct ligation (p<0.05). Nei ther pancreatic duct ligation nor stimulation of pancreatic exocrine secret ion with cholecystokinin octapeptidelsecretin alone resulted in acute pancr eatitis. Topical carbachol stimulated sphincter of Oddi motility abolished trans-sphincteric dow, and increased pancreatic exocrine secretion (p<0.05) and pancreatic duct pressure to levels comparable with pancreatic duct lig ation (p<0.001). Carbachol application (with or without combined peptide st imulation) 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-Induced sphincter of Oddi dysfunction when coupled with stimulat ed pancreatic secretion causes acute pancreatitis. This may be an important pathophysiological mechanism causing various forms of acute pancreatitis.