Differential effect of stress on gastric somatostatin, prostaglandin E2 and gastrin release in the rat

G. Pizzuto, D. Surgo, M. Clementi, R. Marsico, A. Genco, A. Materia, N. Basso

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)143-147
Number of pages5
JournalItalian Journal of Gastroenterology and Hepatology
Volume29
Issue number2
Publication statusPublished - 1997

Fingerprint

Gastrins
Somatostatin
Dinoprostone
Stomach
Gastric Mucosa
Isoproterenol
Aspirin
Histology
Carbachol
Portal Vein
Radio
Ulcer
Prostaglandins
Sprague Dawley Rats
Buffers
Peptides
Acids
Wounds and Injuries

Keywords

  • Gastrin
  • Prostaglandin E
  • Somatostatin
  • Stress ulcer

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Differential effect of stress on gastric somatostatin, prostaglandin E2 and gastrin release in the rat. / Pizzuto, G.; Surgo, D.; Clementi, M.; Marsico, R.; Genco, A.; Materia, A.; Basso, N.

In: Italian Journal of Gastroenterology and Hepatology, Vol. 29, No. 2, 1997, p. 143-147.

Research output: Contribution to journalArticle

Pizzuto, G. ; Surgo, D. ; Clementi, M. ; Marsico, R. ; Genco, A. ; Materia, A. ; Basso, N. / Differential effect of stress on gastric somatostatin, prostaglandin E2 and gastrin release in the rat. In: Italian Journal of Gastroenterology and Hepatology. 1997 ; Vol. 29, No. 2. pp. 143-147.
@article{58b1f0ae6ff143f7af096b14a55fac79,
title = "Differential effect of stress on gastric somatostatin, prostaglandin E2 and gastrin release in the rat",
abstract = "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.",
keywords = "Gastrin, Prostaglandin E, Somatostatin, Stress ulcer",
author = "G. Pizzuto and D. Surgo and M. Clementi and R. Marsico and A. Genco and A. Materia and N. Basso",
year = "1997",
language = "English",
volume = "29",
pages = "143--147",
journal = "Digestive and Liver Disease",
issn = "1590-8658",
publisher = "Elsevier B.V.",
number = "2",

}

TY - JOUR

T1 - Differential effect of stress on gastric somatostatin, prostaglandin E2 and gastrin release in the rat

AU - Pizzuto, G.

AU - Surgo, D.

AU - Clementi, M.

AU - Marsico, R.

AU - Genco, A.

AU - Materia, A.

AU - Basso, N.

PY - 1997

Y1 - 1997

N2 - 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.

AB - 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.

KW - Gastrin

KW - Prostaglandin E

KW - Somatostatin

KW - Stress ulcer

UR - http://www.scopus.com/inward/record.url?scp=0031393258&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031393258&partnerID=8YFLogxK

M3 - Article

VL - 29

SP - 143

EP - 147

JO - Digestive and Liver Disease

JF - Digestive and Liver Disease

SN - 1590-8658

IS - 2

ER -