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EFFECTS OF PROSTAGLANDIN D 2 AND OMEPRAZOLE ON INDOMETHACIN‐INDUCED GASTRIC ULCERS IN RATS
Author(s) -
Fukui Akira,
Nakazawa Saburo,
Goto Hidemi,
Sugiyama Satoru,
Ozawa Takayuki
Publication year - 1988
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1988.tb01037.x
Subject(s) - omeprazole , gastric mucosa , prostaglandin , prostaglandin e , premedication , prostaglandin e2 , medicine , chemistry , pharmacology , gastroenterology , stomach , endocrinology , anesthesia
SUMMARY 1. The mechanism of indomethacin‐induced gastric ulcers was investigated by measuring tissue prostaglandins (PG) levels. 2. The effects of PGD 2 and omeprazole, an H + pump inhibitor, were also estimated. 3. Four kinds of PG—6‐keto PGF 1α , PGF 2α , PGE 2 , and PGD 2 —in rat gastric mucosa were measured by high performance liquid chromatography. 4. All PG levels decreased 1 h after oral administration of 2 mg/kg indomethacin, although they recovered considerably 24 h after administration. No gastric ulcers were observed throughout the experiments in rats treated with 2 mg/kg indomethacin. 5. All PG were not detected 1 h, and even 24 h after administration of 12 mg/kg indomethacin. Over 6 h after administration, gastric ulcers were observed. 6. Premedication with omeprazole prevented ulcer formation, although it did not improve gastric mucosal PG levels. Administration of PGD 2 also reduced ulcer formation, and considerable amounts of PGD 2 in gastric mucosa were detected. 7. It can be concluded that H + is a determining factor in the genesis of indomethacin‐induced gastric ulcers and that persistent decreases in tissue PG levels also participate in ulcer formation.