A new model of chronic visceral hypersensitivity in adult rats induced by colon irritation during postnatal development

Background & Aims The irritable bowel syndrome (IBS) is a common disorder characterized by abdominal pain in the setting of altered perception of viscerosensory stimuli. This so-called visceral hyperalgesia occurs in the absence of detectable organic disease in the peripheral organs and may caus...

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Veröffentlicht in:Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2000-11, Vol.119 (5), p.1276-1285
Hauptverfasser: Al–Chaer, Elie D., Kawasaki, Motohiro, Pasricha, Pankaj J.
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Sprache:eng
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Zusammenfassung:Background & Aims The irritable bowel syndrome (IBS) is a common disorder characterized by abdominal pain in the setting of altered perception of viscerosensory stimuli. This so-called visceral hyperalgesia occurs in the absence of detectable organic disease in the peripheral organs and may cause normal or physiologic contractions to be perceived as painful. Although the pathogenesis of IBS remains speculative and is probably multifactorial, a prevailing paradigm is that transient noxious events lead to long-lasting sensitization of the neural pain circuit, despite complete resolution of the initiating event. Methods Neonatal male Sprague–Dawley rats received either mechanical or chemical colonic irritation between postnatal days 8 and 21 and were tested when they became adults. The abdominal withdrawal reflex and the responses of viscerosensitive neurons were recorded during colon distention. Results Colon irritation in neonates, but not in adults, results in chronic visceral hypersensitivity, with characteristics of allodynia and hyperalgesia, associated with central neuronal sensitization in the absence of identifiable peripheral pathology. Conclusions These results concur largely with observations in patients with IBS, providing a new animal model to study IBS and validating a neurogenic component of functional abdominal pain that encourages novel approaches to health care and research. GASTROENTEROLOGY 2000;119:1276-1285
ISSN:0016-5085
1528-0012
DOI:10.1053/gast.2000.19576