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.