Title: Influence of ondansetron on gastric sensorimotor responses to short duodenal acid infusion in healthy volunteers
Authors: Vanuytsel, Tim ×
Karamanolis, George
Van Oudenhove, Lukas
Vos, Rita
Tack, Jan #
Issue Date: Mar-2011
Publisher: Blackwell Science
Series Title: Neurogastroenterology and Motility vol:23 issue:3 pages:226-232
Duodenal acid infusion induces gastric relaxation and sensitization to distension in healthy volunteers. The acid-sensitive mechanism is still unknown. We hypothesized that 5HT(3)-blockade can inhibit the acid-induced duodenogastric sensorimotor reflex in healthy volunteers.

Fourteen healthy volunteers were included in a randomized, double-blind placebo-controlled cross-over trial. An infusion tube with attached pH-electrode was positioned in the duodenum and a barostat balloon was located in the gastric fundus. Proximal gastric volume and sensitivity to distension were assessed before and during duodenal acid infusion and after pretreatment with intravenous (i.v.) ondansetron (a 5HT(3)-receptor antagonist, 8 mg) or saline. An overall perception score (0-6) and an assessment of nine dyspeptic symptoms by visual analogue scales (VAS) were obtained. Results are given as mean ± SEM.

Ondansetron had no effect on duodenal pH and on the acid-induced increase of proximal gastric volume (increase of 80 ± 20 vs 83 ± 15 mL after ondansetron and placebo; effect of acid <0.001, between treatments ns). After ondansetron, the overall perception score during duodenal acidification and gastric distension was significantly decreased compared with placebo (P=0.01). There was no effect of ondansetron on the individual dyspeptic symptoms.

Ondansetron decreased gastric sensitivity during duodenal acid infusion and gastric distension. 5HT(3)-receptors are involved in acid-induced duodenogastric sensitization, but not in the duodenogastric inhibitory motor reflex.
ISSN: 1350-1925
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Translational Research in GastroIntestinal Disorders
× corresponding author
# (joint) last author

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