Effects of profound duodenogastric reflux on the foregut in rats

Thomas Gasslander; Hidenori Mukaida; Margery K. Herrington; Ronald A. Hinder; Thomas E. Adrian

doi:10.1159/000172537

Effects of profound duodenogastric reflux on the foregut in rats

Thomas Gasslander, Hidenori Mukaida, Margery K. Herrington, Ronald A. Hinder, Thomas E. Adrian

Research output: Contribution to journal › Article › peer-review

1 Citation (Scopus)

Abstract

The trophic effect of pathologic duodenogastric reflux (DGR) was investigated on the esophagus, stomach and pancreas in rats. DGR was induced by split gastrojejunostomy and the effect of omeprazole, cholecystokinin-receptor blockade and gastrin-receptor blockade was studied after 2 weeks. DGR increased plasma cholecystokinin and gastrin and was associated with esophageal hyperplasia and esophagitis, especially in combination with omeprazole. Omeprazole caused an additive rise in gastrin in the DGR group. DGR induced pancreatic growth which was partly inhibited by both cholecystokinin- and gastrin-receptor blockade. Profound DGR has trophic effects on the foregut. Both cholecystokinin and gastrin receptors seem to be involved in the pancreas. The study supports a role for duodenal reflux in esophageal disease and provides possible mechanisms for the trophic effect in the pancreas.

Original language	English
Pages (from-to)	175-182
Number of pages	8
Journal	Digestive Surgery
Volume	14
Issue number	3
DOIs	https://doi.org/10.1159/000172537
Publication status	Published - Jan 1 1997
Externally published	Yes

Keywords

Cholecystokinin
Duodenogastric reflux
Esophagitis
Gastrin
Pancreatic growth
Split gastrojejunostomy

ASJC Scopus subject areas

Surgery
Gastroenterology

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title = "Effects of profound duodenogastric reflux on the foregut in rats",

abstract = "The trophic effect of pathologic duodenogastric reflux (DGR) was investigated on the esophagus, stomach and pancreas in rats. DGR was induced by split gastrojejunostomy and the effect of omeprazole, cholecystokinin-receptor blockade and gastrin-receptor blockade was studied after 2 weeks. DGR increased plasma cholecystokinin and gastrin and was associated with esophageal hyperplasia and esophagitis, especially in combination with omeprazole. Omeprazole caused an additive rise in gastrin in the DGR group. DGR induced pancreatic growth which was partly inhibited by both cholecystokinin- and gastrin-receptor blockade. Profound DGR has trophic effects on the foregut. Both cholecystokinin and gastrin receptors seem to be involved in the pancreas. The study supports a role for duodenal reflux in esophageal disease and provides possible mechanisms for the trophic effect in the pancreas.",

keywords = "Cholecystokinin, Duodenogastric reflux, Esophagitis, Gastrin, Pancreatic growth, Split gastrojejunostomy",

author = "Thomas Gasslander and Hidenori Mukaida and Herrington, {Margery K.} and Hinder, {Ronald A.} and Adrian, {Thomas E.}",

year = "1997",

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doi = "10.1159/000172537",

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AU - Gasslander, Thomas

AU - Mukaida, Hidenori

AU - Herrington, Margery K.

AU - Hinder, Ronald A.

AU - Adrian, Thomas E.

PY - 1997/1/1

Y1 - 1997/1/1

N2 - The trophic effect of pathologic duodenogastric reflux (DGR) was investigated on the esophagus, stomach and pancreas in rats. DGR was induced by split gastrojejunostomy and the effect of omeprazole, cholecystokinin-receptor blockade and gastrin-receptor blockade was studied after 2 weeks. DGR increased plasma cholecystokinin and gastrin and was associated with esophageal hyperplasia and esophagitis, especially in combination with omeprazole. Omeprazole caused an additive rise in gastrin in the DGR group. DGR induced pancreatic growth which was partly inhibited by both cholecystokinin- and gastrin-receptor blockade. Profound DGR has trophic effects on the foregut. Both cholecystokinin and gastrin receptors seem to be involved in the pancreas. The study supports a role for duodenal reflux in esophageal disease and provides possible mechanisms for the trophic effect in the pancreas.

AB - The trophic effect of pathologic duodenogastric reflux (DGR) was investigated on the esophagus, stomach and pancreas in rats. DGR was induced by split gastrojejunostomy and the effect of omeprazole, cholecystokinin-receptor blockade and gastrin-receptor blockade was studied after 2 weeks. DGR increased plasma cholecystokinin and gastrin and was associated with esophageal hyperplasia and esophagitis, especially in combination with omeprazole. Omeprazole caused an additive rise in gastrin in the DGR group. DGR induced pancreatic growth which was partly inhibited by both cholecystokinin- and gastrin-receptor blockade. Profound DGR has trophic effects on the foregut. Both cholecystokinin and gastrin receptors seem to be involved in the pancreas. The study supports a role for duodenal reflux in esophageal disease and provides possible mechanisms for the trophic effect in the pancreas.

KW - Cholecystokinin

KW - Duodenogastric reflux

KW - Esophagitis

KW - Gastrin

KW - Pancreatic growth

KW - Split gastrojejunostomy

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JO - Digestive Surgery

JF - Digestive Surgery

IS - 3

ER -

Effects of profound duodenogastric reflux on the foregut in rats

Abstract

Keywords

ASJC Scopus subject areas

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