Role of endogenous gastric mucosal prostaglandins in the formation of acute gastric mucosal lesions induced by aspirin, ethanol, HCl and CH3COOH.
The role of endogenous mucosal prostaglandins (PGs) in the production of acute gastric mucosal lesions (AGML) was examined in rats. Aspirin, ethanol or 0.6 N-HCl was given intragastrically and 20% acetic acid was injected into the gastric wall. Endogenous gastric mucosal PG (A + B), PGE and PGF were determined by radioimmunoassay. Their gastric contents were markedly reduced by aspirin administration (p less than 0.001). The level of gastric mucosal PGs still remained low (p less than 0.001) after the aspirin-induced AGML began to heal. Furthermore, rats with AGML induced by ethanol, HCl or acetic acid, showed no decrease in endogenous gastric mucosal PGs compared with the controls. These findings indicated that endogenous PGs are not necessary for either the induction or healing of experimental AGML.
D000085:Acetates / Q000008:administration & dosage / Q000633:toxicity*; D000208:Acute Disease; D000284:Administration, Oral; D000818:Animals; D001241:Aspirin / Q000008:administration & dosage / Q000633:toxicity*; D000431:Ethanol / Q000008:administration & dosage / Q000633:toxicity*; D005753:Gastric Mucosa / Q000378:metabolism / Q000473:pathology*; D006851:Hydrochloric Acid / Q000008:administration & dosage / Q000633:toxicity*; D008297:Male; D011453:Prostaglandins / Q000378:metabolism*; D011454:Prostaglandins A / Q000378:metabolism; D011456:Prostaglandins B / Q000378:metabolism; D011458:Prostaglandins E / Q000378:metabolism; D011460:Prostaglandins F / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology
D000085:Acetates; D011453:Prostaglandins; D011454:Prostaglandins A; D011456:Prostaglandins B; D011458:Prostaglandins E; D011460:Prostaglandins F; D000431:Ethanol; D006851:Hydrochloric Acid; D001241:Aspirin