Prevention of ethanol and aspirin-induced gastric mucosal lesions by paracetamol and salicylate in rats: role of endogenous prostaglandins

Gut. 1982 Jun;23(6):536-40. doi: 10.1136/gut.23.6.536.

Abstract

Paracetamol or sodium salicylate given intragastrically 30 minutes before the administration of absolute ethanol or acidified aspirin dose-dependently reduced the formation of mucosal lesions. The generation of gastric mucosal prostaglandin-like activity increased with ethanol and was completely suppressed by acidified aspirin. Paracetamol or sodium salicylate given alone increased the generation of mucosal prostaglandin-like material. Indomethacin, the prostaglandin synthesis inhibitor, suppressed this effect and inhibited the protective influence of paracetamol or sodium salicylate on the production of gastric lesions.

MeSH terms

  • Acetaminophen / therapeutic use*
  • Animals
  • Aspirin
  • Epoprostenol / biosynthesis
  • Epoprostenol / physiology*
  • Ethanol
  • Female
  • Gastric Mucosa / drug effects*
  • Gastric Mucosa / metabolism
  • Indomethacin / pharmacology
  • Male
  • Prostaglandins / physiology*
  • Rats
  • Rats, Inbred Strains
  • Sodium Salicylate / therapeutic use*
  • Stomach Ulcer / chemically induced
  • Stomach Ulcer / metabolism
  • Stomach Ulcer / prevention & control*

Substances

  • Prostaglandins
  • Acetaminophen
  • Ethanol
  • Epoprostenol
  • Aspirin
  • Sodium Salicylate
  • Indomethacin