Plasma corticosterone and restraint induced gastric pathology: Age-related differences after administration of corticotropin releasing factor

Bakke, Hans Kristian; Murison, Robert

doi:10.1016/0024-3205(89)90205-1

Cited by 17 publications

(4 citation statements)

References 31 publications

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“…Moreover, Murison et al (30) have observed that metyrapone treatment, which slightly reduced corticosterone levels under stress, had no effect on erosions and concluded that the findings do not support a simple causal relationship between adrenocortical activity and gastric ulceration. Recently, corticosterone secretion during stress has been considered to be a correlational phenomenon rather than a causal factor in gastric pathology (3). In contrast, based on our previous (8)(9)(10)(11) and present findings we suggest that an acute increase of corticosterone during stress is a potent gastroprotective component of the hormonal response to stress.…”

Section: G1027contrasting

confidence: 74%

Corticosterone increase inhibits stress-induced gastric erosions in rats

Filaretova

Filaretov

Makara

1998

American Journal of Physiology-Gastrointestinal and Liver Physi

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The role of glucocorticoids released in response to stress in the pathogenesis of stress-induced gastric erosions has been reevaluated. Gastric erosions elicited in male rats by 3-h cold-restraint or water-restraint stresses were studied after acute reduction of corticosterone release or occupation of glucocorticoid receptors by the antagonist RU-38486 during stress. Stress-induced corticosterone production was reduced by creating a lesion on the hypothalamic paraventricular nucleus (PVN) 4 days before stress as well as by pretreatment with a rabbit antiserum to adrenocorticotropin (ACTH) 30 min before stress. RU-38486 (10 mg/kg po) was administered 20 min before and 60 min after the onset of stress. Corticosterone for replacement was injected 15 min before the onset of stress to mimic stress-induced corticosterone response. Plasma corticosterone levels were measured by fluorometry or RIA. Gastric erosions were quantitated by measuring the area of damage. Four days after PVN lesion, stress-induced corticosterone release was decreased and gastric erosions were increased. Injecting corticosterone significantly attenuated the effect of PVN lesion on gastric erosions. The ACTH antiserum inhibited corticosteroid secretion in response to stress and markedly increased gastric erosions. The administration of the glucocorticoid/progesterone antagonist RU-38486 significantly potentiated the formation of stress-induced gastric erosions. These observations support the suggestion that glucocorticoids released during stress have a gastroprotective action rather than an ulcerogenic effect as was generally accepted.

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Section: G1027contrasting

confidence: 74%

Corticosterone increase inhibits stress-induced gastric erosions in rats

Filaretova

Filaretov

Makara

1998

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…However, after CRF administration, only the young animals had a significant increase in plasma corticosterone levels, and post-restraint gastric ulcerations were more severe in older rats. The increased corticosterone secretion during stress is related to the increased occurrence of gastric lesions but it is not the sole causative agent for the pathogenesis of gastric lesions [28]. However, this suggests a new role of corticosterone produced during stress in gastric ulceration.…”

Section: Discussionmentioning

confidence: 99%

The effects of palm vitamin E on stress hormone levels and gastric lesions in stress-induced rats

Ibrahim¹,

Kamisah²,

Nafeeza³

et al. 2012

aoms

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IntroductionThis study examines the effects of palm vitamin E (PVE) or α-tocopherol (α-TF) supplementation on adrenocorticotropin hormone (ACTH), corticosterone and gastric lesions in rats exposed to water-immersion restraint stress (WIRS).Material and methodsSixty male Sprague-Dawley rats (200-250 g) were divided into three groups. Group I: 20 rats as a control group were given a normal diet. Group II: 20 rats received oral supplementation of PVE at 60 mg/kg body weight. Group III: 20 rats received oral supplementation of α-TF at 60 mg/kg body weight. After the treatment period of 28 days, each group was further subdivided into two groups: 10 rats not exposed to stress, and the other 10 rats subjected to WIRS for 3.5 h. Blood samples were taken to measure the ACTH and corticosterone levels. The rats were then sacrificed and the stomach excised and opened along the greater curvature and examined for lesions.ResultsRats exposed to WIRS had lesions in their stomach mucosa. Our findings showed that dietary supplementation of PVE or α-TF was able to reduce gastric lesions significantly in comparison to the stressed controls. The WIRS increased plasma ACTH and corticosterone significantly. Palm vitamin E and α-TF treatments reduced these parameters significantly compared to the stressed controls.ConclusionsSupplementation with either PVE or α-TF reduces the formation of gastric lesions, probably by inhibiting the elevation of ACTH and corticosterone levels induced by stress.

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“…46 Stomachs were washed in ice cold saline and opened along the greater curvature to wash the interior with phosphate buffered saline for scoring gastric ulcers as the sum of their cumulative length in mm per stomach with the aid of a magnifying lens and a micrometer. 56 All samples were coded and blindly scored. Because of the protective effect of food against SU, stomachs containing food remnants were excluded regardless of their ulcer scores.…”

Section: Animal Experimentsmentioning

confidence: 99%

Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs

et al. 2002

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When exposed to prolonged stress, rats develop gastric ulceration, enhanced colon motility with depletion of its mucin content and signs of physiological and behavioral arousal. In this model, we tested whether antidepressants (fluoxetine and bupropion), anxiolytics (diazepam and buspirone) or the novel nonpeptide corticotropin-releasing hormone (CRH) type-1 receptor (CRH-R1) antagonist, antalarmin, modify these responses. Fluoxetine, bupropion, diazepam and antalarmin all suppressed stress-induced gastric ulceration in male SpragueDawley rats exposed to four hours of plain immobilization. Antalarmin produced the most pronounced anti-ulcer effect and additionally suppressed the stress-induced colonic hypermotility, mucin depletion, autonomic hyperarousal and struggling behavior. Intraperitoneal CRH administration reproduced the intestinal but not the gastric responses to stress while vagotomy antagonized the stress-induced gastric ulceration but not the intestinal responses. We conclude that brain CRH-R1 and vagal pathways are essential for gastric ulceration to occur in response to stress and that peripheral CRH-R1 mediates colonic hypermotility and mucin depletion in this model. Nonpeptide CRH-R1 antagonists may therefore be prophylactic against stress ulcer in the critically ill and therapeutic for other pathogenetically related gastrointestinal disorders such as peptic ulcer disease and irritable bowel syndrome.

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Plasma corticosterone and restraint induced gastric pathology: Age-related differences after administration of corticotropin releasing factor

Cited by 17 publications

References 31 publications

Corticosterone increase inhibits stress-induced gastric erosions in rats

Corticosterone increase inhibits stress-induced gastric erosions in rats

The effects of palm vitamin E on stress hormone levels and gastric lesions in stress-induced rats

Marked suppression of gastric ulcerogenesis and intestinal responses to stress by a novel class of drugs

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