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Experimental studies on the pathogenesis of gastric mucosal lesions induced by indomethacin in Lewis rats
Ist Teil von
Japanese Journal of Pharmacology, 1999, Vol.79 (suppl.1), p.53-53
Ort / Verlag
The Japanese Pharmacological Society
Erscheinungsjahr
1999
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
We previously reported that Lewis (L) rat is an indomethacin (IND)-ulcer-prone strain. To determine the mechanism of the ulcers in L rats, the influences of IND on gastric acid secretion and gastric mucosa were examined in the present study. [Materials and Methods] IND was administered to L-and Wistar-rats which had been fasted overnight. The pylorus was ligated 2 hrs after IND dosing. Two hours later, the stomach was removed to measure the acidity. Rabeprazole, a proton pump inhibitor, at 1mg/kg (s.c.), and teprenone, a gastric mucosal defensive agent, at 60mg/kg (p.o.), had been administered 1hr prior to IND dosing. [Results] IND (4 to 25mg/kg, p.o.) increased gastric acid secretion, and enhanced the severity of mucosal lesions in a dose-dependent manner in L rats. However Wistar rats showed no such tendency. Rabeprazole inhibited the influence of IND on both the gastric acid secretion and mucosal lesions. On the other hand, teprenone did not affect acid secretion, but inhibited mucosal lesions. [Conclusion] These observations may reflect some strain differences in ulcerogenesis with IND. They also indicate that acid plays an important role in the pathogenesis of IND-induced gastric mucosal lesions, in addition to disruption of defence mechanisms such as cytoprotection.