Bile-pancreatic juice replacement not cholinergic-and cholecystokinin-receptor blockade reverses acinar cell hyperstimulation after bile-pancreatic duct ligation - 11/09/11
This study was presented at the Tenth Annual Meeting of the Society for Surgery of the Alimentary Tract/Ross Laboratories Residents and Fellows Research Conference, La Jolla, California, May 13, 1995, and at the 36th Annual Meeting of the Society for Surgery of the Alimentary Tract, San Diego, California, May 14–17, 1995. It was previously published as an abstract [Am J Surg 1995;169:455].
Abstract |
Background |
Acinar cell inhibitors (eg, atropine) fail to ameliorate clinical and experimental acute pancreatitis. We hypothesized that amelioration of pancreatic acinar cell hyperstimulation after bile and pancreatic duct ligation is better with gut replacement of bile and pancreatic juice than with cholinergic- and cholecystokinin (CCK)-receptor blockade.
Methods |
Using acinar cell amylase activity as an index of hyperstimulation, we studied 63 rats in two sets of experiments. Bile-pancreatic juice exclusion from gut—without (set one) and with (set two) bile and pancreatic duct obstruction— was treated with atropine and CCK-receptor antagonist L-364,718, or with enterai replacement of bile-pancreatic juice.
Results |
In the set one experiment, acinar cell hyperstimulation after bile-pancreatic; juice exclusion was reversed by combined L-364,718 and atropine pretreatment. In set two, acinar cell hyperstimulation after bile and pancreatic duct ligation was reversed by enterai bile and pancreatic juice replacement, but not by combined L-364,718 and atropine pretreatment.
Conclusions |
According to this experimental corollary of early gallstone impaction, prevention of acinar cell hyperstimulation after duct occlusion should be aimed at the source of the response to bile-pancreatic juice exclusion, namely, the gut, rather than at the target of the response, the pancreatic acinar cell.
El texto completo de este artículo está disponible en PDF.| * | This work was supported by a Merit Review Grant from Medical Research Service, Department of Veterans Affairs, Washington, D.C.; and by a Research Fellowship (IS) from the Department of Surgery, Northwestern University Medical School, Chicago, Illinois. |
Vol 171 - N° 1
P. 207-211 - janvier 1996 Regresar al número
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