Open AccessInhibition of Heidenhain Pouch Pepsin Secretion by Commercial Cholecystokinin and Duodenal Fat in Dogs
Author(s) -
Sumio Nakajima,
D. F. Magee
Publication year - 1974
Publication title -
annals of surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.153
H-Index - 309
eISSN - 1528-1140
pISSN - 0003-4932
DOI - 10.1097/00000658-197408000-00020
Subject(s) - pentagastrin , cholecystokinin , methacholine , pepsin , medicine , endocrinology , secretion , pouch , gastric acid , chemistry , biochemistry , anatomy , enzyme , receptor , respiratory disease , lung
In unanesthetized dogs with Heidenhain pouches and separated duodenal pouches, intravenous infusion of commercial cholecystokinin (1.0 IDU per min) produced a significant depression of pouch acid and pepsin secretion stimulated by pentagastrin (1.0 microg per min) or by methacholine (2.0 microg per min). Acid response to methacholine was temporarily augmented. Irrigation of the duodenal pouches with emulsified fat produced similar patterns of depression of acid secretion in response to pentagastrin and pepsin secretion in response to pentagastrin or methacholine. Acid secretion stimulated by methacholine was temporarily augmented after the irrigation. It is concluded that fat releases endogenous cholecystokinin from the duodenal mucosa and that cholecystokinin, or duodenal fat, powerfully depresses Heidenhain pouch pepsin secretion in dogs. The involvment of the gastric inhibitory polypeptide (GIP) cannot be assessed from the present experiments.