Effects of Ecabet Sodium (TA-2711), a New Antiulcer Agent, on Gastrointestinal Mucosal Prostanoid Production and Morphology in Rats

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Effects of ecabet sodium (TA-2711), a locally acting antiulcer agent, on prostanoid production and the morphology of the rat gastrointestinal mucosa were studied in comparison with sucralfate. Ecabet, at therapeutic doses (25 and 100 mg/kg, p.o.), dose-dependently increased the gastric mucosal level of prostaglandin E_2 (PGE_2) : sucralfate (100 mg/kg, p.o.) showed a tendency to increase the PGE_2 level. In an ex vivo study, ecabet (25 and 100 mg/kg, p.o.) dose-dependently increased the capacity of the gastric mucosa to synthesize PGE_2 and PGI_2 without modifying tromboxane A_2 (TXA_2) synthesis, and the 100 mg/kg dose persisted for up to 3 h. Ecabet (400 mg/kg, p.o.) also significantly increased PGE_2 synthesis and there was a tendency to increase PGI_2 synthesis by the duodenal mucosa, without affecting TXA_2 synthesis. PGE_2 synthesis by the colonic mucosa was not affected, even at a high dose of ecabet (1000 mg/kg, p.o.). When the rat gastric mucosa was examined by light microscopy and scanning electron microscopy, ecabet (100 and 400 mg/kg, p.o.) had caused no morphological change to the gastric mucosa, while sucralfate (100 and 400 mg/kg, p.o.) produced apical rupture of the epithelial cells and subepithelial edema. The present study indicates that ecabet locally stimulates PGE_2 and PGI_2 production in the gastroduodenal mucosa and this effect is not attributable to a local irritant action accompanied by superficial epithelium damage.
社団法人日本薬学会の論文
1993-12-15

Effects of Ecabet Sodium (TA-2711), a New Antiulcer Agent, on Gastrointestinal Mucosal Prostanoid Production and Morphology in Rats

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