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  • 1
    ISSN: 1573-2568
    Keywords: prostaglandins ; indomethacin ; quality of ulcer healing ; recurrence ; gastric ulcer ; polymorphonuclear cell
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The study was performed to examine whether indomethacin administered during the initial period of acetic acid-induced gastric ulcer healing affects future ulcer recurrence. Gastric ulcers were produced in rats by subserosal injection of acetic acid. Indomethacin (1 mg/kg/day, orally) administered either alone or concomitant with ornoprostil (50µg/kg/day, orally) was started on the fourth day and continued for 56 days. In rats whose ulcer healed at the 90th day after production of ulcer, endoscopy was done every 30 days to examine recurrence of ulcer. Gastric specimens were obtained 10, 30, 60, 90, and 240 days after ulcer production for histology, to quantitate the height of regenerated mucosa, thickness of fibrous tissue, degree of polymorphonuclear cell infiltration, and PAS-positive cells. Cumulative ulcer recurrence rate was significantly higher in rats initially treated with indomethacin than in controls. Increased polymorphonuclear cell infiltration was the major histologic abnormality persisting after cessation of indomethacin. Ornoprostil reversed these abnormalities caused by indomethacin. In conclusion, the administration of indomethacin during the initial period of the ulcer healing promoted persistent polymorphonuclear cell infiltration and increased ulcer recurrence rates, possibly via a prostaglandin-dependent mechanism.
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  • 2
    ISSN: 1573-2568
    Keywords: indomethacin ; prostaglandin ; blood flow ; gastric mucosa ; mucosal damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of 16,16-dimethyl prostaglandin E2 PGE2 on gastric mucosal blood flow and gastric mucosal damage were tested in rats given indomethacin. Blood flow was measured by hydrogen gas clearance. Indomethacin given intragastrically reduced the blood flow in nonlesion areas and the levels of PGE2 and 6-keto-PGF1α in the gastric mucosa and caused mucosal damage in a dose-related way. Indomethacin (20 mg/kg) significantly reduced the blood flow 30 min after administration, and the reduction increased until 90 min. Then the flow plateaued until 240 min. Gastric mucosal damage caused by 20 mg/kg of indomethacin and evaluated by only gross observations, began at 60 min and developed with time until 240 min after administration. 16,16-Dimethyl PGE2 (5 μg/kg) did not affect the reduction of blood flow caused by indomethacin during 240 min of measurements, but it significantly inhibited the indomethacin-induced mucosal damage evaluated by gross observations. These results suggest that prevention by 16,16-dimethyl PGE2 of grossly observed gastric mucosal damage caused by indomethacin was not related by preservation of the gastric mucosal blood flow in the areas without lesions.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1573-2568
    Keywords: zinc ; zincl-carnosine ; gastric mucosa ; prostaglandin ; indomethacin ; cytoprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of zincl-carnosine on ethanol-induced damage and the correlation of these effects with endogenous prostaglandin E2 were evaluated in rat gastric mucosain vivo andin vivo. When given either intragastrically or intraperitoneally, zincl-carnosine (10 or 30 mg/kg) prevented gross visible damage to gastric mucosa caused by ethanol without affecting the mucosal prostaglandin E2 level. This protective effect of zincl-carnosine was not inhibited by indomethacin. Histological assessment showed that zincl-carnosine inhibited deep mucosal necrosis, as did 16,16-dimethyl-prostaglandin E2. Zincl-carnosine (10−6 or 10−5 M) inhibited the damage caused by ethanol to gastric cells isolated from rat gastric mucosain vivo; this effect was not inhibited by indomethacin. The results suggested that zincl-carnosine protects the gastric mucosa and enhances cellular resistance to ethanol without the mediation of endogenous prostaglandins.
    Type of Medium: Electronic Resource
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