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AJP - Gastrointestinal and Liver Physiology, Vol 245, Issue 1 85-G91, Copyright © 1983 by American Physiological Society
ARTICLES |
A. S. Fink and J. H. Meyer
To study interactions between intraduodenal acid and emulsified oleic acid, dogs with chronic gastric and pancreatic fistulas received two sets of intestinal perfusates. The first set contained HCl plus bovine serum albumin (BSA) with or without 20 mM oleic acid. The BSA and HCl were varied so that each 50 ml contained 1, 2, or 4 meq of acid titratable from an initial pH of 2.0 or 3.5 to an end-point pH of 4.5. Oleic acid significantly enhanced pancreatic bicarbonate and protein outputs induced by acidified BSA. In additional studies, a less soluble protein solution, a 1:1 mixture of bovine hemoglobin and ovalbumin (HB-OV), was utilized. Fixed amounts of HCl (1, 2, or 4 meq/50 ml) were added to native or pepsin-digested HB-OV solution with or without 20 mM oleic acid. In these studies, initial pH and titratable acid (to end-point pH 4.5) varied with the nature of the HB-OV (undigested or digested), as well as with the amount of HCl added. Under these conditions, digested HB-OV and oleic acid potentiated acid-induced bicarbonate output, but only in those solutions with the greatest amount of added HCl. Acid-induced bicarbonate or protein outputs were not further augmented upon combination of HB-OV digests with oleic acid. We conclude that acid-induced pancreatic bicarbonate secretion is potentiated by intraduodenal protein digests and emulsified fatty acids.
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