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Gut 2002;51(Supplement 1):i19-i23; doi:10.1136/gut.51.suppl_1.i19
Copyright © 2002 BMJ Publishing Group Ltd & British Society of Gastroenterology.
Gut 2002;51:i19-i23
© 2002 by Gut

VISCERAL PERCEPTION

Visceral perception: inflammatory and non-inflammatory mediators

L Bueno, J Fioramonti

Department of Neurogastroenterology and Nutrition, Institut National de la Recherche Agronomique, Neurogastroenterology Unit INRA, 180 Chemin de Tournefeville, BP3 31931 Toulouse Cedex 9, France

Correspondence to:
Correspondence to:
Dr L Bueno, Department of Pharmacology INRA, 180 Chemin de Tournefeuille, BP3, 31931 Toulouse Cedex 9, France;
lbueno{at}toulouse.inra.fr

ABSTRACT

Visceral hypersensitivity is currently the most widely accepted mechanism responsible for abdominal pain. Inflammatory mediators are known to sensitise primary afferents and to recruit silent nociceptors. Recent evidence suggests that non-inflammatory mediators also have the potential to trigger visceral pain. This sequence of events may constitute part of an alerting system which prompts the central nervous system to correct gastrointestinal responses to ingestion.

Keywords: visceral hypersensitivity; pain mediators; inflammation; stress; mast cells

Abbreviations: ATP, adenosine triphosphate; CGRP, calcitonin gene related peptide; CNS, central nervous system; IBS, irritable bowel syndrome; IL, interleukin; NGF, nerve growth factor; NKA, neurokinin A; PGE 2; prostaglandin E2; SP, substance P; TNF, tumour necrosis factor; 5-HT, serotonin


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