Paracetamol confers resistance to ethanol-induced gastric mucosal damage in rats.
Paracetamol given orally or subcutaneously did not produce any observable gastric mucosal damage, nor did it change the acidity of the residual secretion in rat stomachs. However, it delayed the gastric emptying rate and increased the residual volume of gastric secretion. Pretreatment with paracetamol 250 mg kg-1 significantly prevented ethanol-induced gastric ulceration. Although it did not influence ethanol-stimulated acid secretion, it increased the mucosal mucus content in the ethanol-treated animals. The findings suggest that the protective mechanism of paracetamol against ethanol-induced damage is likely to be due to improved gastric mucosal integrity, through an increase in the adherent mucosal mucus which protects the underlying delicate cellular structures.
Poon
Y K
YK
Department of Pharmacology, Faculty of Medicine, University of Hong Kong.
Cho
C H
CH
Ogle
C W
CW
D000082:Acetaminophen / Q000494:pharmacology*; D000818:Animals; D000431:Ethanol / Q000037:antagonists & inhibitors / Q000633:toxicity*; D005753:Gastric Mucosa / Q000166:cytology / Q000187:drug effects / Q000473:pathology*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D013276:Stomach Ulcer / Q000139:chemically induced / Q000517:prevention & control*
D000082:Acetaminophen; D000431:Ethanol