A new model for production of chronic gastric ulcer by duodenogastric reflux in rats.
We have established an experimental model of chronic gastric ulcer, in rats which transection of the lower horizontal portion of the duodenum and anastomosis of the forestomach to the upper part of the jejunum caused regurgitation of all duodenal juice into the stomach. After 3, 6, 12, and 30 wk, all treated rats developed an ulcer in the prepyloric region on the lesser curvature of the stomach. More than half of the antrum was finally involved in the ulcer. Histologic studies revealed chronic ulcers quite similar to human ones. As a control series, transection at the pylorus failed to produce an ulcer. Although many papers have appeared regarding the experimental production of chronic gastric ulcer, most of the studies reported have applied chemicals, drugs, or mechanical injury to the gastric mucosa. Our model produced chronic regurgitation of duodenal juice as a natural phenomenon, and uniformly resulted in ulcer formation. Intragastric total bile acid concentrations were significantly elevated in the reflux group. Serum gastrin levels, the thickness of the fundic mucosa, and the height of fundic gland were also significantly increased. Thus, the detergent action of bile acids and the increased acid secretion were assumed to play an important role in ulcer formation. Further studies using this model are warranted on the pathogenesis of chronic peptic ulceration.
D000818:Animals; D001647:Bile Acids and Salts / Q000032:analysis; D002908:Chronic Disease; D004195:Disease Models, Animal; D004383:Duodenogastric Reflux / Q000150:complications*; D005753:Gastric Mucosa / Q000473:pathology; D005755:Gastrins / Q000097:blood; D006863:Hydrogen-Ion Concentration; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000209:etiology*
D001647:Bile Acids and Salts; D005755:Gastrins