UNLABELLED: A humoral factor may mediate the intestinal phase of gastric acid secretion. An ex vivo perfused segment of canine jejunum maintained by an oxygenated asanguinous physiologic perfusate was used to test for release of an enterooxyntin (EO) in response to balloon distention at 30 mm Hg for 15 min. Gastric acid secretion in guinea pig fundic mucosa was determined indirectly by a quantitative cytochemical bioassay (CBA) of oxyntic cell hydroxyl ion production (HIP). An increase in the optical density (OD) caused by the cytochemical stain in the oxyntic cells reflects HIP, an index of acid secretion. Basal OD for segments with distention was 16.6 +/- 0.53 and for those without 15.5 +/- 0.68 (NS). Results are expressed as mean change of OD from basal (mean delta OD +/- SEM). (Table-see text) EO caused greater stimulation of HIP than gastrin or histamine. EO was heat stable. Trichloroacetic acid treatment decreased EO activity as did pronase digestion suggesting that EO is composed of one or more peptides. CONCLUSION: EO, an acid secretagogue, is a humoral agent probably composed of one or more peptides and is released by small bowel distention. Mechanical distention of the small bowel may be an important mechanism for the perpetuation of gastric acid secretion. The ex vivo perfused jejunal segment in conjunction with the CBA are ideal tools with which to study mechanisms of release of EO and the mechanism of action of EO on the oxyntic cell.
UNLABELLED: A humoral factor may mediate the intestinal phase of gastric acid secretion. An ex vivo perfused segment of canine jejunum maintained by an oxygenated asanguinous physiologic perfusate was used to test for release of an enterooxyntin (EO) in response to balloon distention at 30 mm Hg for 15 min. Gastric acid secretion in guinea pig fundic mucosa was determined indirectly by a quantitative cytochemical bioassay (CBA) of oxyntic cell hydroxyl ion production (HIP). An increase in the optical density (OD) caused by the cytochemical stain in the oxyntic cells reflects HIP, an index of acid secretion. Basal OD for segments with distention was 16.6 +/- 0.53 and for those without 15.5 +/- 0.68 (NS). Results are expressed as mean change of OD from basal (mean delta OD +/- SEM). (Table-see text) EO caused greater stimulation of HIP than gastrin or histamine. EO was heat stable. Trichloroacetic acid treatment decreased EO activity as did pronase digestion suggesting that EO is composed of one or more peptides. CONCLUSION: EO, an acid secretagogue, is a humoral agent probably composed of one or more peptides and is released by small bowel distention. Mechanical distention of the small bowel may be an important mechanism for the perpetuation of gastric acid secretion. The ex vivo perfused jejunal segment in conjunction with the CBA are ideal tools with which to study mechanisms of release of EO and the mechanism of action of EO on the oxyntic cell.
Authors: M O Hamed; A D Barlow; N Dolezalova; S Khosla; A Sagar; F M Gribble; S Davies; M P Murphy; S A Hosgood; M L Nicholson; K Saeb-Parsy Journal: BJS Open Date: 2021-03-05