Stress-induced changes in intestinal transit in the rat: A model for irritable bowel syndrome

Williams, Christopher S.; Villar, Rodrigo; Peterson, Julie; Burks, Thomas F.

doi:10.1016/0016-5085(88)90231-4

Cited by 243 publications

(181 citation statements)

References 21 publications

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“…2 Less severe, prolonged stress has been implicated in the pathogenesis of peptic ulcer disease 3 and irritable bowel syndrome (IBS). 4 appear to be interrelated and to be associated with affective and anxiety disorders. 5,6 Moreover, early life adversity is associated with more prevalence of mood and anxiety disorders 7,8 as well as predisposition to gastric ulceration 9 and IBS 10 later in adulthood.…”

Section: Introductionmentioning

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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Section: Introductionmentioning

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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“…In addition to the change in stool consistency, polycarbophil accelerated intestinal luminal transit, producing increased fecal weight in the first 8 h after dosing in naive and constipated rats. There is also the possibility that polycarbophil delayed intestinal luminal transit in the diarrhea models, as polycarbophil decreased stool output stimulated by WRS, which increases stool output by altering intestinal transit without increasing fecal water content (11). Further investigation regarding the effect of polycarbophil on intestinal luminal transit should be done.…”

Section: Discussionmentioning

confidence: 99%

“…To investigate the effect of drugs on stress-accelerated defecation, rats were subjected to WRS, a model of stress-related intestinal dysfunction without ulcer formation in IBS (11,12). Rats were anesthetized lightly with ether and their shoulders, upper forelimbs and thoracic trunks were wrapped in cloth tape to restrict, but not prevent, movement.…”

Section: Wrs Model Defecation In Ratsmentioning

confidence: 99%

“…The animals awoke within 5 min and immediately moved about in their individual cages. The experiments were carried out between 4:00 and 6:00 PM to avoid any circadian influence on stool excretion (11). One hour after administration of the test drug or vehicle, rats were subjected to WRS for 1 h. Williams et al (11) reported that all feces were formed and dry, and restraint stress did not result in diarrhea; therefore, the wet weight of the fecal pellets expelled during the following hour was determined.…”

Section: Wrs Model Defecation In Ratsmentioning

confidence: 99%

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Laxative and Anti-diarrheal Activity of Polycarbophil in Mice and Rats

Saito

Mizutani

Iwanaga

et al. 2002

Japanese Journal of Pharmacology

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ABSTRACT-We investigated the laxative and anti-diarrheal activity of polycarbophil, an insoluble hydrophilic polymer, in comparison with other agents used for treating functional bowel disorder (FBD). In naive rats, polycarbophil (500 mg /kg) increased fecal weight and water contents without producing diarrhea. Carboxymethylcellulose (CMC) did not produce evident changes in bowel movement. Picosulfate markedly produced diarrhea. Loperamide, trimebutine and granisetron decreased stool output dose-dependently. Constipation, indicated by decrease in fecal weight, was produced by loperamide and clonidine in rats. Polycarbophil (500 mg /kg) and CMC increased fecal weight without diarrhea. Conversely trimebutine further decreased fecal weight in constipated rats. Polycarbophil (500 mg /kg) suppressed diarrhea induced by castor oil, and at 250 -500 mg /kg, it produced shaped stools in animals with stools loosened by prostaglandin E2, serotonin or carbachol in mice. Polycarbophil (500 mg /kg) also reduced stools in rats with stool output increased by wrap restraint stress (WRS). CMC had no effect in the diarrhea models, except for carbachol-induced diarrhea, and WRS-induced evacuation. Loperamide, trimebutine and granisetron inhibited diarrhea production and WRS-induced evacuation, except for carbachol-induced diarrhea. The results show that polycarbophil prevents constipation and diarrhea without inducing diarrhea or constipation, which is different from the other agents. Hydrophilic polymers such as polycarbophil will be promising agents for the treatment of FBD.

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“…9 Inhibition of gastric emptying, gastric secretion, gastric contraction and stimulation of colonic motility and defecation have now been well established in adult rats as the hallmarks of neurovisceral motor responses to stressors of psychological, physical, chemical and immunological origin. [10][11][12][13] Members of stress hormone family, more specifically corticotrophin-releasing factor (CRF) and urocortin, have been shown to mimic multifaceted acute responses to stress. 8 Both hormones mediate their actions through CRF-receptor subtype 1 (CRF-R1) and CRF-receptor subtype 2 (CRF-R2).…”

Section: Introductionmentioning

confidence: 99%

Mechanism(s) of in utero meconium passage

Lakshmanan

Ross

2008

J Perinatol

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To use sheep and rat models and demonstrate that stressors activate fetal glucocorticoid (GC) system, corticotrophin-releasing factor (CRF) system and cholinergic neurotransmitter system (ChNS) leading to propulsive colonic motility and in utero meconium passage. Immunohistochemical studies (IHS) were performed to localize GC-Receptors, CRF-receptors and key molecules of ChNS in sheep fetal distal colon. CRF expression in placenta and enteric endocrine cells in fetal rat system were examined and the effects of acute hypoxia on in utero meconium passage was tested. IHS confirmed localization and gestation dependent changes in GC-Rs, CRF-Rs and cholinergic markers in sheep fetal colon. Rat placenta and enteric endocrine cells express CRF and gastrointestinal tract express CRF-Rs. Hypoxia is a potent inducer of meconium passage in term fetal rats. Stress is a risk factor for in utero meconium passage and laboratory animal models can be used to develop pharmacotherapy to prevent stress-induced in utero meconium passage.

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Stress-induced changes in intestinal transit in the rat: A model for irritable bowel syndrome

Cited by 243 publications

References 21 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

Laxative and Anti-diarrheal Activity of Polycarbophil in Mice and Rats

Mechanism(s) of in utero meconium passage

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