抄録
Non-steroidal antiinflammatory drugs (NOSAID) produce the gastric mucosal lesions by inhibiting prostaglandin (PG) synthesis in the gastric mucosa. We tested the ulcerogenicity and the potential of PG inhibition with tiaprofen and indomethacin in a same antiinflammatory dose (ED50 on the carrageenin-induced foot edema) in rats. The animals were intragastrically given tiaprofen three times before sacrifice in a dose of 6 mg/kg or indomethacin in a dose of 4 mg/kg. Endogenous PGE2 and prostacyclin in fundic and antral mucosa were determined by radioimmunoassay. Tiaprofen (3 times of 6 mg/kg, i.g.) is less potent than indomethacin (3 times of 4 mg/kg, i.g.) to produce the gastric mucosal lesions (ulcer index, 6.6±1.0 vs. 20.6±2.9, significantly different at P<0.005) . Gastric mucosal PGE2 is completely decreased in a same degree by either tiaprofen or indomethacin. However, the decrease of mucosal prostacyclin is significantly (fundus; P<0.025, antrum; P<0.005) less in tiaprofen-treated rats than in indomethacin treated one. These results suggest that the ulcerogenicity of tiaprofen is less potent than indomethacin, and this difference may cause from the mucosal prostacyclin levels.
