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Cholecystokinin octapeptide increases rectal sensitivity to pain in healthy subjects
Author(s) -
Sabaté JM.,
Gorbatchef C.,
Flourié B.,
Jian R.,
Coffin B.
Publication year - 2002
Publication title -
neurogastroenterology and motility
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.489
H-Index - 105
eISSN - 1365-2982
pISSN - 1350-1925
DOI - 10.1046/j.1365-2982.2002.00370.x
Subject(s) - distension , cholecystokinin , medicine , barostat , irritable bowel syndrome , nociception , basal (medicine) , anesthesia , visceral pain , saline , stimulation , compliance (psychology) , sensory system , endocrinology , receptor , psychology , insulin , social psychology , cognitive psychology
Hypersensitivity during rectal distension has been demonstrated in irritable bowel syndrome (IBS). Studies performed in animals and indirect data in humans suggest that cholecystokinin (CCK) could modulate visceral sensations. The aim of this study was to assess the effects of i.v. infused sulphated cholecystokinin octapeptide (CCK‐OP) on rectal sensitivity in response to distension. In eight healthy subjects, rectal sensitivity and compliance were determined during a randomized double‐blind study, with four sessions each separated by 7 days. Sensory thresholds and rectal compliance were assessed during slow‐ramp (40 mL min −1 ) and rapid‐phasic distensions (40 mL s −1 , 5 mmHg stepwise, 1‐min duration), and were compared before and during continuous infusion of either saline or CCK‐OP at 5, or 20 or 40 ng kg −1 h −1 . During rapid phasic distension but not during slow ramp distension, CCK‐OP at 40 ng kg −1 h −1 produced a significant decrease in sensory thresholds compared with the basal period. Rectal compliance was not modified by any infusion. At pharmacological doses, CCK‐OP decreases sensory thresholds during rapid phasic distension that may preferentially stimulate serosal mechanoreceptors, but has no effect on mucosal mechanoreceptors stimulated during slow ramp distensions. Modulation of rectal sensitivity by CCK could be implicated in the pathogenesis of the rectal hypersensitivity observed in IBS.