Stress Ulcer Model Research Articles

187 - A new experimental model of stress ulcer in rats and the effects of psychotropic and autonomic drugs.

187 - A new experimental model of stress ulcer in rats and the effects of psychotropic and autonomic drugs.

A new model of stress ulcer in the rat with pylorus ligation and its pathogenesis.

Water-immersion stress for 7, 14, or 20 hr consistently induced linear or punctate stress ulcers (mucosal erosions) in the corpus of the stomach in intact rats. When the pylorus of the stomach had been ligated prior to stressing, the stress ulcers changed their morphological feature (mainly punctate and in one place elongated) and location (both in corpus and antrum). Histologically, the stress ulcer developed in the proximal antrum of pylorus ligated rats and penetrated into the muscularis mucosa. Sodium bicarbonate, chlorpromazine, hexamethonium, atropine, metiamide, and bilateral vagotomy markedly inhibited the stress ulcers which developed in the pylorus-ligated rats. Phentolamine and propranolol hardly affected the development of stress ulcers. Amylopectine evoked a new type of stress ulcer in the corpus when it was given to the pylorus-ligated rats.

Gastric mucosal ischemia in experimental stress ulcer

The pathogenesis of gastric ulceration that occasionally follows major blood loss remains unclear. Localized gastric ischemia is one of several classic explanations [9]. Gastroscopic evidence that focal gastric mucosal ischemia may precede stress ulceration has recently been reported [7]. Visible ischemia has not been correlated with measurements of local mucosal blood flow clinically or in the laboratory. This is a quantitative study of the patterns of blood flow in the stomach of a reliable, experimental stress ulcer model [lo]. Using isotopically labeled microspheres we demonstrated patches of disproportionate mucosal ischemia at sites of subsequent ulceration.

Gastric blood flow in endotoxin-induced stress ulcer.

The effect of endotoxin shock on the distribution of gastric blood flow was measured with radioactive microspheres in a swine stress ulcer model. Ten piglets were shocked with intravenously administered Escherichia coli endotoxin and compared with six controls. Blood flow was calculated before and after shock by assaying 2-cm square sections of stomach. Distribution of gastric blood flow was analyzed graphically and ischemic regions were compared to ulcerated areas. Endotoxin caused a redistribution of gastric blood flow which did not parallel cardiac output change. Ischemia was maximum in the corpus where flow per gram decreased 62.2%, and stress ulcers developed only in this region in all shocked animals. There were no ulcers in controls where gastric blood flow paralleled cardiac output. Endotoxin caused a selective regional gastric ischemia unlike the diffuse, patchy flow seen following hemorrhage.

A Swine Stress Ulcer Model

A Swine Stress Ulcer Model