Cortisone acetate and stress on the healing process of chronic gastric ulcer in rats

Okabe, Susumu; Saziki, Ryuichi; Takagi, Kazuo

doi:10.1152/jappl.1971.30.6.793

Cited by 22 publications

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“…We studied the sensitivity of acetic acid ulcers induced in rats to stress in order to determine whether or not stress exerts an effect on the ulcer healing process. 28) Water-immersion stress (20 h) performed at various intervals after acetic acid ulcer induction evoked stress ulcers in the glandular portion, but did not aggravate the acetic acid ulcers. Intermittent cold stress (4°C) 10 h daily for 1 week also failed to exacerbate the acetic acid ulcers.…”

Section: Characteristic Features Of Acetic Acid Ulcersmentioning

confidence: 94%

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Okabe

Amagase

2005

Biological & Pharmaceutical Bulletin

208

166

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Four types of experimental chronic ulcer models, named acetic acid ulcer models, have been developed to examine the healing process of peptic ulcers, screen anti-ulcer drugs, and better evaluate the adverse effects of various anti-inflammatory drugs on the gastrointestinal mucosa. The model easily and reliably produces round, deep ulcers in the stomach and duodenum, allowing acetic acid ulcer production in mice, rats, Mongolian gerbils, guinea pigs, cats, dogs, miniature pigs, and monkeys. These ulcer models highly resemble human ulcers in terms of both pathological features and healing process. The models have been established over the past 35 years and are now used throughout the world by basic and clinical scientists. One of the characteristic features of acetic acid ulcers in rats is the spontaneous relapse of healed ulcers Ͼ100 d after ulceration, an endoscopically confirmed phenomenon. Indomethacin significantly delays the healing of acetic acid ulcers, probably by reducing endogenous prostaglandins and inhibiting angiogenesis in ulcerated tissue. Helicobacter pylori significantly delays healing of acetic acid ulcers and causes relapse of healed ulcers at a high incidence in Mongolian gerbils. Anti-secretory drugs (e.g. omeprazole), prostaglandin analogs, mucosal defense agents (e.g. sucralfate), and various growth factors all significantly enhance healing of acetic acid ulcers. Gene therapy with epidermal growth factor and vascular endothelial growth factor applied to the base of acetic acid ulcers in rats is effective in enhancing ulcer healing. Since an inhibitor of nitric oxide syntase prevents ulcer healing, nitric oxide might be involved in the mechanism underlying ulcer healing. We conclude that acetic acid ulcer models are quite useful for various studies related to peptic ulcers.

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Section: Characteristic Features Of Acetic Acid Ulcersmentioning

confidence: 94%

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Okabe

Amagase

2005

Biological & Pharmaceutical Bulletin

208

166

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“…In addition, there have been several reports that such agents can significantly or tend to cause reulceration of partially healed or healed gastric ulcers (12)(13)(14). Okabe et al (12) reported that cortisone, administered at 25 or 75 mg/kg for 10 to 20 days, starting from the 50th day af ter ulceration, tended to aggravate partially healed acetic acid-induced ulcers.…”

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confidence: 99%

“…Okabe et al (12) reported that cortisone, administered at 25 or 75 mg/kg for 10 to 20 days, starting from the 50th day af ter ulceration, tended to aggravate partially healed acetic acid-induced ulcers. Kahn et al (13) and Ito et al (14) reported that cortisone (25 mg/kg) or hydrocortisone (20 mg/kg) administered for 10 to 20 days starting from the 50th or 40th day after ulceration induced by thermocau tery or acetic acid injection in rats apparently caused the ulcers to recur.…”

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confidence: 99%

Effects of Indomethacin and Prednisolone on the Different Stages of Healing of Acetic Acid-Induced Gastric Ulcers in the Rat

Ogihara

Okabe

1993

Japanese Journal of Pharmacology

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ABSTRACT-Repeated administration of indomethacin or prednisolone for 2 weeks apparently delayed the healing of initial gastric ulcers induced by acetic acid injection in rats. While indomethacin significantly in terfered with the healing of partially healed 2-week-old ulcers, prednisolone did not. Indomethacin had no effect on the healing of "unhealed" 4-week-old ulcers. However, prednisolone significantly enhanced the healing of such "unhealed" ulcers, and it decreased the weight of the connective tissue at the ulcer base and the collagen content. These results suggest that prednisolone enhances the healing of "unhealed" gastric ulcers by degrading the fibroplasia that had amply developed in the connective tissue.Keywords: Prednisolone, Fibroplasia, Ulcer (acetic acid-induced) Various non-steroidal or steroidal anti-inflammatory agents delay the healing of gastric ulcers induced in ex perimental animals (1-4). Decreases in the endogenous prostaglandin level (3, 4) and the gastric mucosal blood flow around ulcers (5) and the inhibition of angiogenesis in the granulation tissue (6) have been postulated to be involved in the underlying mechanism. In addition, we proposed that the amply developed fibroplasia at the ulcer base on indomethacin treatment could interfere with the contraction of the ulcer, thereby resulting in clearly demarcated ulcers (designated as "unhealed" ulcers) (7). If so, it is conceivable that the degradation of this fibro plasia might accelerate the healing of unhealed ulcers. Steroidal anti-inflammatory agents decrease the collagen content and/or the weight of pre-existing granulation tis sue such as carrageenin granuloma tissue (8). Therefore, we examined the effect of prednisolone as well as that of indomethacin on the spontaneous healing of 2-week-old ulcers and 4-week-old "unhealed" ulcers.Male Donryu rats (Nihon SLC), weighing 240-260 g, were used. The rats were fasted for 5 hr prior to ulcer production to facilitate the injection of the acetic acid so lution into the gastric wall. Gastric ulcers were induced by submucosal injection of 20% acetic acid (0.03 ml) into the border between the antrum and corpus on the anterior wall of the stomach (9). After closure of the abdomen, the rats were maintained in the usual manner. Since well defined, deep ulcers were observed 5 days after the acid in jection, we defined the 5th day as the day of ulceration. After ulceration, the rats were randomly divided into the following 3 groups. a) Indomethacin (Sigma) at 1 mg/kg or prednisolone (Sigma) at 5 mg/kg was administered sub cutaneously once daily (9:00 AM) for 4 or 2 weeks after ul ceration, respectively. Preliminary experiments indicated that treatment with prednisolone for more than 2 weeks significantly reduced the body weight of rats, and their general physical state was poor. Therefore, experiments with prednisolone were done only with a 2-week treat ment. Control animals received the vehicle alone. b) In domethacin at 1 mg/kg or prednisolone at 5 mg/kg was administered subcutaneously once da...

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“…On the other hand, it was reported that cortisone aggravated the healing process of chronic gastric ulcers (2,11,(13)(14)(15), but exerted no aggravating effects on completely healed gastric ulcers (2).…”

Section: Discussionmentioning

confidence: 99%

Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice.

Watanabe

Hagiwara

1980

Jpn.J.Pharmacol

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Abstract-The influence of various ulcerogenic treatments on healing gastric ulcers induced by thermocautery was studied in mice. A low dose of serotonin (5HT) which did not produce ulceration, was found to aggravate gastric ulcers at 15th or 30th day after thermocauterization, but other ulcerogenic treatments including histamine, norepinephrine, vasopressin, acetic acid ingestion and cold-restraint stress did not affect this induced gastric ulcer. Bleeding and ulceration, however, occurred in the gastric glandular portion in addition to thermocauterization ulcer by the treatment of acetic acid ingestion or cold-restraint stress. Histological sections of gastric ulcers (15th and 30th day) 24 hr after 5HT injection, showed severe necrosis of the re generated mucosal layer. Microvessel structure in the gastric mucosa as revealed by the Indian-ink infusion, showed a local obstruction of blood flow on the edge of ulcers 1 or 3 hr after 5HT injection. Although acetic acid ingestion increased trans mucosal fluxes of Na+ and K+, 5HT had no effect on the ion flux in normal mice. Thus the healed ulcer area was resistant to various ulcerogenic stimulants, except for 5HT, and the vasoactive factor of 5HT may be involved in the aggravating process of gastric ulcers induced by thermocautery.

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Cortisone acetate and stress on the healing process of chronic gastric ulcer in rats

Cited by 22 publications

References 0 publications

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

Effects of Indomethacin and Prednisolone on the Different Stages of Healing of Acetic Acid-Induced Gastric Ulcers in the Rat

Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice.

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Cortisone acetate and stress on the healing process of chronic gastric ulcer in rats

Cited by 22 publications

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An Overview of Acetic Acid Ulcer Models<br>&mdash;The History and State of the Art of Peptic Ulcer Research&mdash;

An Overview of Acetic Acid Ulcer Models<br>&mdash;The History and State of the Art of Peptic Ulcer Research&mdash;

Effects of Indomethacin and Prednisolone on the Different Stages of Healing of Acetic Acid-Induced Gastric Ulcers in the Rat

Aggravating effect of serotonin on gastric ulceration induced by thermocautery under the healing process in mice.

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An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—

An Overview of Acetic Acid Ulcer Models<br>—The History and State of the Art of Peptic Ulcer Research—