This study was designed to determine if gastric somatostatin is released during the acidification of the duodenal bulb or distal duodenum. A proximal duodenal pouch was per f used with HCl in normal laparotomized anesthetized dogs during an intravenous infusion of saline, pentagastrin (5 µg/kg/hr), or histamine (20 µg/kg/hr). Bulb acidification during i.v. saline was accompanied by a slight increase in antral vein somatostatin-like immunoreactivity (SLI), but no change in fundic vein SLI or inferior vena caval SLI levels occurred. Acidification of the bulb during i.v. pentagastrin elicited an increase in fundic vein SLI from a baseline level of 593 ± 205 pg/ml to a peak level of 1,554 ± 510 pg/ml (P < 0.02), and antral vein SLI again increased slightly. Inferior vena caval SLI did not change. Acidification of the bulb during the infusion of histamine did not alter fundic vein, antral vein, or inferior vena caval SLI levels. Perfusion of a more distal duodenal pouch during the infusion of pentagastrin did not change fundic vein SLI but elicited a rise in antral vein SLI levels; inferior vena caval SLI did not change. The data demonstrate that in dogs, the acidification of the duodenal bulb during the intravenous infusion of pentagastrin, but not of histamine or saline, is accompanied by a marked increase in fundic SLI levels. Acidification of a more distal duodenal pouch during pentagastrin infusion does not provoke this response. Fundic somatostatin, stimulated by as yet unidentified signals from the acidified duodenal bulb, could, therefore, be a mediator of the previously described “bulbogastrone mechanism” and act as a local inhibitor of gastric acid secretion.
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