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Original Article

Duodenal Acidification and Jejunal Hyperosmolality Inhibit Pentagastrin-Stimulated Acid Secretion in Chronic Gastric Fistula Rats

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Pages 1095-1101 | Received 03 Mar 1989, Accepted 11 May 1989, Published online: 08 Jul 2009
 

Abstract

In chronic gastric fistula (GF) rats, HC1 and a hyperosmolal solution of polyethylene glycol (PEG) in the upper intestine inhibit pentagastrin-stimulated gastric acid secretion by different mechanisms, but their anatomic sites have not yet been established. In the present study GF rats were provided with Thiry-Vella loops of the duodenum and the bile and pancreatic ducts transplanted to the proximal jejunum, or with Thiry-Vella loops of the proximal jejunum. In the latter rats the duodenum was anastomosed as a blind loop to the jejunum to prevent any gastric juice from entering the duodenum. Duodenal loop perfusion with 0.20 M HC1 inhibited the acid response to pentagastrin by 62%, but perfusion with 1200mOsmol × kg-1 of PEG solution did not alter the response. In contrast, acidification of the proximal jejunal loop did not alter but hyperosmolality inhibited the response by 41%. The study shows that the mechanism for inhibition by intestinal acidification is confined to the duodenum and that for inhibition by hyperosmolality is located in the proximal jejunum–but whether only to the proximal part is unknown.

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