From simplicity to complexity (1950–1990): the case of peptic ulceration—II. Animal studies.

Weiner, Herbert

doi:10.1097/00006842-199109000-00002

Cited by 14 publications

(4 citation statements)

References 129 publications

(186 reference statements)

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“…65 By virtue of its extensive projections to brain nuclei that participate in the neurocircuitry of stress, the vagal efferents are well positioned to mediate the gastric responses to stress. 66 Indeed, the stomach receives by far more vagal innervation (both afferent and efferent) than any other viscus. 67 Efferent vagal fibers contain a variety of neurotransmitters that could be ulcerogenic, eg TRH, serotonin and opiate peptides.…”

Section: Discussionmentioning

confidence: 99%

“…CRH is extensively distributed in the hypothalamus and limbic system nuclei that project to the dorsal motor nucleus of the vagus (DMV) and CRH containing nerve fibers are found in the DMV. 66,67 The effects of antalarmin in attenuating colonic responses to stress were also marked. It significantly suppressed both colonic hypermotility and mucin depletion.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

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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“…The distribution of CRF in the hypothalamus is well documented, and its effect on the stress response through the hypothalamic-pituitary-adrenal (HPA) axis has been extensively studied (Vale et al, 1981;Rivier et al, 1982;Orth et al, 1983;Dunn and Berridge, 1990;De Souza, 1995). Central administration of CRF increases mean arterial pressure and heart rate (Fisher et al, 1982), and CRF inhibits gastric acid secretion and gastric emp-tying (Druge et al, 1989;Weiner, 1991). Central administration of CRF increases mean arterial pressure and heart rate (Fisher et al, 1982), and CRF inhibits gastric acid secretion and gastric emp-tying (Druge et al, 1989;Weiner, 1991).…”

Section: Crf; Astrocyte; Cerebellum; Developmentmentioning

confidence: 99%

Corticotropin releasing factor induces proliferation of cerebellar astrocytes

Bishop

King

et al. 2000

J. Neurosci. Res.

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“…One showed, for instance, that among recent-onset ulcer patients given the exhaustive and stringently scored Bedford College Life Events and Difficulties Scale (4), the rate of severe life difficulties during the six months preceding ulcer development was five times higher than that in controls carefully matched from the electoral rolls for age, sex and socioeconomic status (5). Similarly, though doubts remain as to the relevance of animal models to human peptic ulcer, the extensive animal literature (6,7) shows unequivocally that not only physical stressors (8) but also purely psychological manipulations (6) can cause or facilitate erosion of the gastric and sometimes the duodenal mucosa in mammals ranging from rats to monkeys (9).…”

Section: Thesis: Psychosocial Risk Factorsmentioning

confidence: 99%

Peptic Ulcer at the End of the 20th Century: Biological and Psychological Risk Factors

Levenstein

1999

Canadian Journal of Gastroenterology and Hepatology

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The prevailing concept of peptic ulcer etiology has swung over entirely in just a few years from the psychological to the infectious, yet the rich literature documenting an association between psychosocial factors and ulcer is not invalidated by the discovery of Helicobacter pylori. Physical and psychological stressors interact to induce ulcers in animal models, concrete life difficulties and subjective distress predict the development of ulcers in prospective cohorts, shared catastrophes such as war and earthquakes lead to surges in hospitalizations for complicated ulcers, and stress or anxiety can worsen ulcer course. Many known ulcer risk factors, including smoking, nonsteroidal anti-inflammatory drug use, heavy drinking, loss of sleep and skipping breakfast, can increase under stress; the association of low socioeconomic status with ulcer is also accounted for in part by psychosocial factors. Among possible physiological mechanisms, stress may induce gastric hypersecretion, reduce acid buffering in the stomach and the duodenum, impair gastroduodenal blood flow, and affect healing or inflammation through psychoneuroimmunological mechanisms. Psychosocial factors seem to be particularly prominent among idiopathic or complicated ulcers, but they are probably operative in run of the mill H pylori disease as well, either through additive effects or by facilitating the spread of the organism across the pylorus, while gastrointestinal damage by nonsteroidal anti-inflammatory drugs can also be potentiated by stress. Although the clinical importance of peptic ulcer is fading along with the millennium, due to secular trends and new therapies, it remains worthy of study as a splendid example of the biopsychosocial model.

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From simplicity to complexity (1950–1990): the case of peptic ulceration—II. Animal studies.

Cited by 14 publications

References 129 publications

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

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

Corticotropin releasing factor induces proliferation of cerebellar astrocytes

Peptic Ulcer at the End of the 20th Century: Biological and Psychological Risk Factors

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