Stomach, Glandular Stomach - Ulcer

Spontaneous occurrence of ulceration of the glandular stomach is uncommon in NTP studies in mice and F344/N rats. Ulceration is seen primarily in treated rats and has been experimentally induced as a model for ulcer in humans. An ulcer (Figure 1 and Figure 2) is defined as the loss of the entire epithelial thickness down to or through the basement membrane and muscularis mucosa, whereas an erosion (see Stomach, Glandular Stomach - Erosion ) is a partial thickness loss of epithelium. In comparison, necrosis of epithelium is diagnosed instead of ulceration if the necrotic epithelium is still present and at least partially attached to the underlying lamina propria. Bacterial infections can occur secondary to erosion or ulceration due to local trauma from a gavage procedure or necrosis/ischemia. Indigenous bacteria in the stomach of the rat are normally found adherent to only the most luminal mucosa but not in the gastric pits. Following erosion/ulceration, bacteria can gain access to deeper portions of the mucosa and stomach wall. Compounds that produce erosions and ulcers can act via effects on mucosal blood flow, mucosal cell kinetics, mucus or acid/bicarbonate secretion, or maintenance of the mucus barrier. High-fat diets, chronic pantothenic acid deficiency, deficiency of gluconeogenic amino acids, platelet-activating factor, increased reflux of bile salts, and reduced exocrine pancreatic function are associated with ulceration but only with intact vagal innervations. The mediators of ulceration may be metabolites of the lipooxygenase pathway of arachidonic acid metabolism. Pharmaceutical agents that are leukotriene blockers prevent ulceration by some ulcerogens.