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  Vol. 125 No. 12, December 1990 TABLE OF CONTENTS
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  PAPERS READ BEFORE THE 14TH ANNUAL SURGICAL SYMPOSIUM OF THE ASSOCIATION OF VETERANS AFFAIRS SURGEONS, CHARLESTON, SC, MAY 7 TO 9, 1990
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Amelioration of Cholinergic-Induced Pancreatitis With a Selective Cholecystokinin Receptor Antagonist

Anton J. Bilchik, MD; Karl A. Zucker, MD; Thomas E. Adrian, PhD, MRC(Path); Irvin M. Modlin, MD, PhD

Arch Surg. 1990;125(12):1546-1549.


Abstract

• Acute edematous pancreatitis follows excessive cholinergic stimulation in patients exposed to anticholinesterase-containing insecticides. We describe the role of cholecystokinin and the benefits of cholecystokinin receptor blockade in this form of pancreatitis. A cholinergic mimetic (carbachol) was administered to rats weighing 300 to 350 g and produced a form of edematous pancreatitis that mimics that seen in humans. Animals received carbachol intraperitoneally, either alone (250 µg/kg of body weight) or with cholecystokinin-receptor antagonist devazepide (3 mg/kg of body weight) and were killed 4 hours later. Carbachol administration resulted in a 19% increase in pancreatic weight, a fourfold increase in serum amylase levels, and a 14-fold increase in serum lipase levels. Plasma cholecystokinin levels, however, were not altered. Devazepide administered prior to cholinergic hyperstimulation blocked pancreatic weight increase and reduced elevations in serum amylase levels twofold and lipase levels fourfold. Although cholecystokinin levels are not elevated in this model of pancreatitis, blockade of even low, background concentrations of this regulatory peptide is beneficial.

(Arch Surg. 1990;125:1546-1549)



Author Affiliations

From the the Department of Surgery, Yale University School of Medicine, New Haven, Conn (Drs Bilchik and Modlin); the Department of Surgery, University of Maryland School of Medicine, Baltimore, and Baltimore Veterans Affairs Hospital (Dr Zucker); and the Department of Surgery, Creighton University, Omaha, Neb (Dr Adrian).


Footnotes

Accepted for publication August 11, 1990.

Read before the 14th Annual Surgical Symposium of the Association of Veterans Affairs Surgeons, Charleston, SC, May 7, 1990.

Reprint requests to University of Maryland Medical Center, 22 S Greene St, Baltimore, MD 21218 (Dr Zucker).



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THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Cholecystokinin induction of mob-1 chemokine expression in pancreatic acinar cells requires NF-kappa B activation
Han and Logsdon
Am. J. Physiol. Cell Physiol. 1999;277:C74-C82.
ABSTRACT | FULL TEXT  





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