A study of the actions of naloxone and morphine on gastric acid secretion and gastric mucosal damage in the rat

A. Debreceni, B. Debreceni, Gy Mózsik

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

There exists a considerable controversy in the literature with regard to the effect of either opiate receptor blockade or that of morphine in different gastric and intestinal ulcer models in the rat. We performed experiments to evaluate the effects of naloxone and morphine on gastric acid secretion and gastric mucosal damage in different experimental models of gastric mucosal injury, namely in indomcthacin-, HCl (0.6N)- and ethanol (96%)-models. We found that: 1) 10 mg/kg naloxone ip given twice, effectively protected gastric mucosa against indomethacin (30 mg/kg ip) and against the acid-dependent injury caused by 0.6 N HCl (1 mL, ig), but not against the non acid-dependent injury caused by 96% ethanol (1 mL ig); 2) morphine (10 + 10 mg/kg ip) increased ulcers in the HCl model, but had no effect in the two other models; 3) this ulcer-aggravating effect of morphine in the HCl-model was blocked by pretreatment of 2 mg/kg ip naloxone; and 4) both naloxone (5 + 5 and 10 + 10 mg/kg ip) and morphine (10 + 10 mg/kg ip) significantly decreased gastric acid secretion in l-h pylorus ligated rats. We conclude that: 1) naloxone dose-dependently protects against the indomethacin- and HCl-, but not against the ethanol-induced gastric mucosal damage; 2) morphine aggravates the HCl-induced ulcerogenesis; and 3) both opioid receptor agonist and antagonist decrease gastric acid secretion.

Original languageEnglish
Pages (from-to)189-197
Number of pages9
JournalJournal of Physiology Paris
Volume91
Issue number3-5
DOIs
Publication statusPublished - Jan 1 1997

Keywords

  • Gastric acid secretion
  • Gastric mucosal injury
  • Gastric mucosal protection
  • Morphine
  • Naloxone

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology (medical)

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