Background. The relationship between gastric mucosal damage induced by stress, peptides present in the gastric mucosa and is not clear. Aim of this study was to determine whether cold-restraint stress affected the release of gastric somatostatin, gastrin and in the isolated perfused stomach preparation. Methods. Male Sprague-Dawley rats were used, 12 cold-restraint stressed and 12 unstressed controls. 4 additional unstressed rats were treated with aspirin (100 mg/kg p.o.). After 30 minutes, isolated stomachs were perfused for 50 minutes with Krebs-Ringer buffer additioned with isoproterenol or carbamycholine plus somatostatin-14 or carbamylcholine alone. somatostatin, gastrin and prostaglandin E2 release in the portal vein effluent were measured by radio-immuno-assay. Histology of the gastric mucosa was obtained from a further 4 stressed and 4 unstressed rats. Results. In the stomach from stressed animals, the somatostatin response to isoproterenol and the prostraglandin E2 response to carbamylcholione plus somatostatin were significantly lower than in the controls, whereas gastrin response to carbamylcoline was enhanced by stress. Treatment with aspirin abolisked the prostraglandin E2 response to stimulation. Gastric mucosa histology from stressed and unstressed animals showed no significant lesions. Conclusions. The inhibition of gastric somatostatin and prostaglandins release coupled to an enhanced acid stimulatory influence appear to antidate gastric mucosal injury and should play a role in the stress ulcer genesis.
|Number of pages||5|
|Journal||Italian Journal of Gastroenterology and Hepatology|
|Publication status||Published - 1997|
- Prostaglandin E
- Stress ulcer
ASJC Scopus subject areas