Influence of age on natural and delayed healing of experimentally-induced gastric ulcers in rats

Penney, Angela G.; Andrews, Fiona; O'Brien, Paul Edmond

doi:10.1007/bf02088755

Cited by 6 publications

(4 citation statements)

References 27 publications

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“…Penney et al 23) examined whether or not age exerts an influence on development and natural or delayed healing of acetic acid ulcers in rats. Penney concluded that there were age-related differences in the development of gastric ulcers, but no age-related differences in natural and indomethacindelayed ulcer healing.…”

Section: Type 3 Ulcer Modelmentioning

confidence: 99%

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: Type 3 Ulcer Modelmentioning

confidence: 99%

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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“…Gastric ulceration induced by acetic acid applied either to the serosa or to the mucosa showed no consistent differences in ulcer size or in ulcer healing in Sprague-Dawley rats aged two to three months, 11 to 12 months or 23 to 24 months (29). In this study, even the administration of indomethacin failed to alter the healing rate of older animals any more than in the younger animals (29). Similarly, Tsukimi and Okabe (28) showed no changes in the healing of gastric ulcers in older rats.…”

Section: Pathophysiologymentioning

confidence: 82%

“…Several studies have not shown an increase in ulcer size after application of injurious agents in older rodents compared with younger rodents (27,28). Gastric ulceration induced by acetic acid applied either to the serosa or to the mucosa showed no consistent differences in ulcer size or in ulcer healing in Sprague-Dawley rats aged two to three months, 11 to 12 months or 23 to 24 months (29). In this study, even the administration of indomethacin failed to alter the healing rate of older animals any more than in the younger animals (29).…”

Section: Pathophysiologymentioning

confidence: 94%

Peptic Disease in Elderly Patients

Khaghan

Holt²

2000

Canadian Journal of Gastroenterology and Hepatology

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The increase in life expectancy demands that more attention be given to gastrointestinal problems, such as peptic ulcer disease, in elderly people. This review summarizes many of the physiological changes that have a role in peptic ulcer disease in elderly patients. How Helicobacter pylori infection modifies the course of peptic disease is also reviewed. The clinical presentation of peptic diseases often differs in elderly people, and atypical symptoms are common. Accurate diagnosis requires aggressive endoscopic evaluation. Treatment regimens using H2 receptor antagonists, proton pump inhibitors and regimens to eradicate H pylori may also need to be altered in elderly patients.

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“…In a previous study, we examined the effect of age on natural ulcer healing and on delayed ulcer healing induced by chronic dosing with indomethacin 1 mg/kg per day 30 . Aged and mature animals showed no reduced capacity for natural ulcer healing.…”

Section: Discussionmentioning

confidence: 99%

Aged gastric mucosa: Mechanisms of vulnerability

Malcontenti‐Wilson

Schulz

Penney

et al. 1998

J of Gastro and Hepatol

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The incidence, frequency of complications and mortality of gastric ulcer disease are increased four‐fold in the elderly taking non‐steroidal anti‐inflammatory drugs (NSAID). There is controversy as to whether this reflects increased usage of NSAID or specific vulnerability associated with age. We have investigated two possible mechanisms for this increase in gastrointestinal effects in the elderly: (i) increased susceptibility to acute gastrotoxicity; and (ii) reduced adaptation to NSAID, in a model of young (2 month), mature (12 month) and aged (24 month) rats. Aspirin damaged 7.7% of the volume of gastric mucosa in the young rat. In mature and aged rats, this increased to 11.3% (P < 0.002 compared to control) and 21.9% (P < 0.005 compared to control), respectively. Thus, aspirin caused a three‐fold increase in the severity of acute gastric mucosal injury in aged animals. However, indomethacin, ibuprofen and L745 337 did not produce any significant acute gastric mucosal damage in 2‐, 12‐ or 24‐month‐old rats. Significant gastric adaptation to diclofenac treatment occurred in both aged and young rats as measured by gastric mucosal damage. The aged gastric mucosa adapted equally as well as the young gastric mucosa to diclofenac. The findings of this study provide only modest support to the hypothesis of increased vulnerability of the stomach in the aged. Aspirin was associated with greater damage in the aged. Adaptation to diclofenac‐induced damage was not reduced in the aged and there was not an increased susceptibility to damage by the non‐aspirin NSAID tested. The selective cyclo‐oxygenase‐2 inhibitor, L745 337, was the least toxic agent and may represent a group of NSAID which cause fewer gastrointestinal complications in the elderly.

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Influence of age on natural and delayed healing of experimentally-induced gastric ulcers in rats

Cited by 6 publications

References 27 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—

Peptic Disease in Elderly Patients

Aged gastric mucosa: Mechanisms of vulnerability

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Influence of age on natural and delayed healing of experimentally-induced gastric ulcers in rats

Cited by 6 publications

References 27 publications

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;

Peptic Disease in Elderly Patients

Aged gastric mucosa: Mechanisms of vulnerability

Contact Info

Product

Resources

About

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—