• Dominique Chassard, Sabine Lansiaux, Frédéric Duflo, François Mion, Nathalie Bleyzac, Richard Debon, and Bernard Allaouchiche.
• Service d'Anesthésie-Réanimation, Hôpital de l' Hôtel-Dieu, Lyon, France. dominique.chassard@chu-lyon.fr
• Anesthesiology. 2002 Jul 1;97(1):96-101.

BackgroundDrugs which accelerate gastric emptying (GE) decrease nausea and vomiting. This could contribute to the antiemetic potential of subhypnotic doses of propofol. On the contrary, subhypnotic doses of propofol used for sedation could decrease GE and thus favor regurgitation and pulmonary inhalation. Therefore, the aim of this study was to assess the effect of low-dose propofol infusion on GE.MethodsOn three separate occasions, 10 volunteers received either a propofol infusion at a rate set to achieve a target plasma concentration of 0.5 microg/ml or equivalent volumes of 10% Intralipid(R) or 0.9% saline. GE for solids was measured by using the octanoic acid breath test. An acetaminophen absorption technique measured the GE rate for liquids. Blood samples were assayed for acetaminophen and propofol. Breath samples were analyzed for (13)CO(2) concentration by isotope-ratio mass spectrometry. Carbon dioxide production (VCO(2)) was measured instead of calculated by indirect calorimetry. Sedation was evaluated by the Bispectral Index of the electroencephalogram.ResultsPropofol blood concentrations were 0.32 +/- 0.20 and 0.45 +/- 0.18 microg/ml at 60 and 165 min, respectively. These concentrations were not sedative. Propofol or its solvent did not modify GE for solids or liquids. In all groups, differences in GE were obtained if measured VCO(2) was integrated in the formula instead of calculated VCO(2) (P < 0.002).ConclusionsSubhypnotic doses of propofol known to be antiemetic do not inhibit GE. These results suggest that the antiemetic properties of propofol are not peripheral and that propofol cannot be considered as a prokinetic agent. V(13)CO(2) must be measured instead of calculated to accurately determine GE.

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