Sulphasalazine and experimental stress ulcers.
The effects of sulphasalazine on gastric ulceration induced by restraint at 4 degrees C (stress) for 2 h were studied in rats. Doses of 63 or 125 mg/kg s.c., which had no effect on stomach wall prostaglandin E2 (PGE2) levels, prevented stress ulceration but not the lesions produced by indomethacin. Stress significantly increased gastric glandular mucosal PGE2 levels. Indomethacin pretreatment (20 mg/kg, p.o.) markedly reduced PGE2 levels in the same region of the stomachs, and worsened stress-induced lesion formation. Pretreatment with sulphasalazine of animals given indomethacin and then subjected to stress did not appear to affect the indomethacin component of indomethacin-stress ulceration. Oral administration of PGE2 200 micrograms/kg significantly elevated gastric PGE2 levels, but had no effect on stress ulceration. It appears that neither the antiulcer activity of sulphasalazine nor stress-induced ulceration is associated with gastric tissue PGE2 increase or decrease, respectively. The protective mechanism may result from the ability of sulphasalazine to inhibit lipoxygenase activity.
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D000284:Administration, Oral; D000818:Animals; D015232:Dinoprostone; D005260:Female; D007213:Indomethacin / Q000008:administration & dosage; D007279:Injections, Subcutaneous; D011458:Prostaglandins E / Q000008:administration & dosage / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D013312:Stress, Physiological / Q000150:complications*; D012460:Sulfasalazine / Q000008:administration & dosage*
D011458:Prostaglandins E; D012460:Sulfasalazine; D015232:Dinoprostone; D007213:Indomethacin