Secretory state of gastric mucosa and its resistance to aspirin injury.
The influence of the secretory status on gastric mucosal tolerance to aspirin injury was assessed in a canine ex vivo model, which provided two segments of mucosa supplied by a single vascular pedicle in the same dog. Acid secretion was stimulated by intravenous infusion of histamine in one mucosa, whereas the secretory response to histamine was significantly impaired by topical treatment with 16,16-dimethyl prostaglandin E2 in the other. As expected, the secreting mucosa exhibited a twofold greater blood flow than the inhibited mucosa. Exposure of both mucosae to 20 mM aspirin for 30 minutes resulted in the appearance of small multiple superficial erosions. The degree of mucosal injury was not significantly different between the secreting and inhibited mucosae. The extent of mucosal damage was similar to that seen when aspirin in acid was placed on resting mucosa in the same model. These data do not support the hypothesis that histamine-stimulated acid secretion and accompanying increase in gastric mucosal blood flow protects the stomach against aspirin injury.
D000818:Animals; D001241:Aspirin / Q000009:adverse effects*; D004285:Dogs; D005753:Gastric Mucosa / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism; D006632:Histamine / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D008863:Microspheres; D011458:Prostaglandins E / Q000494:pharmacology; D012964:Sodium / Q000502:physiology
D011458:Prostaglandins E; D006632:Histamine; D012964:Sodium; D001241:Aspirin