Gastric Antral Ulcers Induced by a Combination of Acid, Indomethacin and Ischemia in Rats

Hirose, Fumiaki; Mizui, Takuji; Shimono, Noriko; Doteuchi, Masami

doi:10.1254/jjp.38.223

Cited by 12 publications

(4 citation statements)

References 14 publications

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“…Although gastric acid aggravates mucosal lesions induced with various noxious agents [22,[35][36][37][38], the protection observed in this study was not achieved by acid inhibition as it could not be intensified by pretreatment with an antisecretory dose of BY. Our obser vation, that an H+K+-ATPase blocker pro tects gastric mucosa is in accord with other authors [39,40].…”

Section: Discussionmentioning

confidence: 82%

Effect of 16.16 Dimethyl Prostaglandin E<sub>2</sub>, N-Acetyl-Cysteine and the Proton Pump Inhibitor BY 831–78 on Hydrogen Peroxide-Induced Mucosal Damage in the Rat Stomach

1990

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Reactive oxygen species are noxious to gastrointestinal mucosa and contribute to a variety of gastrointestinal diseases. We examined whether 16.16 dimethyl prostaglandin E₂ (PG) is protective against the oxidizing action of 6% H₂O₂ causing gross hemorrhagic lesions in rat gastric mucosa. Male Wistar rats were treated with PG, 0.005–5 μg/kg, either intragastrically (i.g.) or subcutaneously, 30 min prior to i.g. administration of 6% H₂O₂, 0.5 ml/100 g. Further animals received 25 mg of the mucus dissolvant N-acetyl-cysteine (NAC) following oral PG treatment or 30 μmol/kg of the H⁺K⁺-ATPase inhibitor BY 831–78 (BY), 4 h before onset of the experiments. Volume, pH and β-N-acetyl-glucosaminidase and lactate dehydrogenase as parameters of cell damage were determined in the gastric juice, i.g. PG treatment achieved 60 and 55 % reduction of the mucosal lesions in doses between 5 and 0.05 μg/kg, respectively, i.p. PG administration was effective in all doses tested. Gastric juice volume was only slightly and enzymes were not significantly affected by PG treatment. NAC did not diminish PG efficacy or aggravate mucosal lesions. Gastric acid suppression did not increase PG-induced protection but was strongly protective by itself, reducing damage by 75%. Low-dose PG treatment achieves an effective protection against oxidative damage in gastric mucosa, which is not the result of dilution or enhanced mucus production.

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Section: Discussionmentioning

confidence: 82%

Effect of 16.16 Dimethyl Prostaglandin E<sub>2</sub>, N-Acetyl-Cysteine and the Proton Pump Inhibitor BY 831–78 on Hydrogen Peroxide-Induced Mucosal Damage in the Rat Stomach

1990

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“…No gastric erosive lesions were observed on and after day 7. (2)(3)(4)(5). Therefore in the present study, we tried to produce an antral ulcer by the combination of 2-DG, aspirin and hy drochloric acid or ammonia solution, avoiding surgical operation; aspirin was substituted for indomethacin because it does not cause intes tinal lesions.…”

Section: Resultsmentioning

confidence: 99%

“…Kolbasa et al (4) reported the indomethacin-induced gastric antral ulcer in hamsters, but the dose was also high. In 1985, Hirose et al (5) reported the rat antral ulcer induced by the combination of acid, in domethacin and ischemia formed by the sur gical operation (ligation of blood vessels). However, this method requires a surgical pro cedure, although the dosage of indomethacin was low.…”

mentioning

confidence: 99%

A Reliable Method for the Production of Antral Gastric Ulcer by a Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats.

1991

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ABSTRACT-In order to establish a reliable method for the production of gastric astral ulcer in rats, combined treatments with three factors: a vagal stimulant, a mucosal barrier breaker and a necrotizing agent were investigated. By the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (100-400 mg/kg, p.o.) and hydrochloric acid (0.15 and 0.35N, 0.5 1.5 ml/100 g, p.o.) or ammonia solution (0.5-1.0%, 0.5-1.5 ml/100 g, p.o.), gastric lesions were prominent ly induced in sites of both the corpus and antrum on day 2. The largest antral ulcer was induced by the combination of 2-DG (200 mg/kg), aspirin (200 mg/kg) and ammonia solution (1%, 10 ml/kg); and the mean antral ulcer index (mm2) was 43.1 ± 4.4 and the incidence was 100%. The antral ulcer was found to penetrate the muscu laris mucosae and still observed on day 21 and day 28 after ulcer induction in a few cases. From these findings, it was indicated that this antral ulcer would be a useful model for studying the etiology and therapy of gastric ulcer disease.

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“…With regard to this, antral ulcer is somewhat different. Several gastric antral ulcer models have been prepared using the rat those produced by simultaneous intravenous infusion of aspirin plus gastric perfusion with HCl [19], by indomethacin in re-feeding [20], by indomethacin plus 2-deoxy-D-glucose [21], and by a combination of HCI, indomethacin, and ischemia [22]. Morphologically, our antral ulcer model is similar to them, but our procedure to produce ulceration is simpler.…”

Section: Discussionmentioning

confidence: 99%

Gastric Antral Ulcer Produced by Diethyldithiocarbamate in Rats

Ishiyama

Yamasaki

Imaizumi

et al. 1988

J. Clin. Biochem. Nutr.

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A subcutaneous dose of diethyldithiocarbamate (DDC) combined with a topical application of hydrochloric acid produced deep ulcers in the lesser curvature of the antrum in pylorus-ligated rats. The ulcers penetrated the tunica muscularis and formed an ulcer with an incidence of 100%. A significant decrease in Cu,Zn-superoxide dismutase (SOD) activity and a significant increase in the level of thiobarbituric acid (TBA) reactants in the antral mucosa occurred prior to the ulcer formation. Treatment with SOD and allopurinol significantly inhibited antral ulceration. These results suggest that superoxide radicals are involved in the pathogenesis of the ulcer and that this ulcer model is useful for studying gastric ulcer etiology.

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Gastric Antral Ulcers Induced by a Combination of Acid, Indomethacin and Ischemia in Rats

Cited by 12 publications

References 14 publications

Effect of 16.16 Dimethyl Prostaglandin E<sub>2</sub>, N-Acetyl-Cysteine and the Proton Pump Inhibitor BY 831–78 on Hydrogen Peroxide-Induced Mucosal Damage in the Rat Stomach

Effect of 16.16 Dimethyl Prostaglandin E<sub>2</sub>, N-Acetyl-Cysteine and the Proton Pump Inhibitor BY 831–78 on Hydrogen Peroxide-Induced Mucosal Damage in the Rat Stomach

A Reliable Method for the Production of Antral Gastric Ulcer by a Combination of 2-Deoxy-D-Glucose, Aspirin and Ammonia in Rats.

Gastric Antral Ulcer Produced by Diethyldithiocarbamate in Rats

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