Increase in pepsin content in gastric mucosa during the course of aspirin- and taurocholate-induced gastric ulceration in rats.
To investigate the possible role of pepsin in ulceration induced by hydrogen ion back-diffusion, the ratio of alkali-labile pepsinogen to total pepsinogen was studied during the course of aspirin- and taurocholate-induced gastric ulceration in comparison with the changes in the ion permeability and histological findings. The results obtained were as follows. (1) The increase in the ulcer index was observed between 1 and 2 hr with intragastric aspirin and between 2 and 4 hr with intragastric taurocholate. (2) The back-diffusion of luminal hydrogen ions, observed as a significant decrease in hydrogen ion net flux, occurred immediately in both cases with aspirin and with taurocholate. (3) A significant increase in the ratio of alkali-labile to total pepsinogen in the homogenate of gastric mucosa was observed at 30 min with aspirin and at 60 min with taurocholate. (4) Histological examination revealed the degeneration of mucosal cells spreading from the luminal surface into the mucosa, which fell off after 120 min with aspirin. These findings indicate that the activated pepsin is involved in the ulcer formation caused by the hydrogen ion back-diffusion, although the origin of the activated pepsin is not clear at the present time.
D000818:Animals; D001241:Aspirin / Q000009:adverse effects; D004058:Diffusion; D005753:Gastric Mucosa / Q000187:drug effects / Q000201:enzymology* / Q000473:pathology; D006863:Hydrogen-Ion Concentration; D008297:Male; D009336:Necrosis; D010434:Pepsin A / Q000378:metabolism*; D010435:Pepsinogens / Q000378:metabolism; D051381:Rats; D013268:Stimulation, Chemical; D013276:Stomach Ulcer / Q000209:etiology*; D013656:Taurocholic Acid / Q000009:adverse effects
D010435:Pepsinogens; D013656:Taurocholic Acid; D010434:Pepsin A; D001241:Aspirin