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. 1980 Nov;192(5):614–619. doi: 10.1097/00000658-198011000-00005

A study of the cholinesterases of the canine pancreatic sphincters and the relationship between reduced butyrylcholinesterase activity and pancreatic ductal hypertension.

T D Dressel, R L Goodale, J W Borner, S Etani
PMCID: PMC1344941  PMID: 7436591

Abstract

Previous work from this laboratory revealed in increased canine pancreatic intraductal pressure following cholinesterase inhibitor intoxication. The pressure was negatively correlated with serum butyrylcholinesterase (BChE) activity, suggesting that BChE activity mediated the pressure rise. This study uses a histochemical technique to investigate the tissue cholinesterase activity of the canine pancreatic sphincters and the effect of a cholinesterase inhibitor (ChEI) on tissue cholinesterase activity. In five control dogs, serial sections of the major and minor spincters were stained for acetylcholinesterase (AChE) and BChE activity. Four treated dogs were given the ChEI, O,O-diethyl-O- (2-isopropyl-6-methyl-4-pyrimidinyl) phosphoro-thioate, 25 mg/kg, one hour prior to excising the ampullae. In the control dogs, BChE activity is present in the periampullary nerves and the pancreatic smooth muscle sphincters. AChE activity is present in nerves but not in smooth muscle. In the treated group, following a dose of ChEI known to cause ductal hypertension, BChE activity was absent in the pancreatic sphincters but AChE activity was preserved in the periampullary nerves. These data suggest that the pancreatic ductal hypertension that occurs following ChEI administration is due to a selective reduction in pancreatic smooth muscle BChE activity.

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These references are in PubMed. This may not be the complete list of references from this article.

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