This Article Résumé de cet Article Full Text Full Text (PDF) Submit a scholarly reply Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Axelsson, P. Articles by Wattwil, M. Search for Related Content PubMed PubMed Citation Articles by Axelsson, P. Articles by Wattwil, M.

Betamethasone does not prevent nausea and vomiting induced by the dopamine-agonist apomorphine

[La bêtaméthasone ne prévient pas les nausées et les vomissements induits par l’agoniste de la dopamine, l’apomorphine]

Patric Axelsson, MD^*, Sven-Egron Thörn, MD PhD, Åsa Lövqvist, RN, Lisbeth Wattwil, RN and Magnus Wattwil, MD PhD

^* From the Departments of Anesthesiology and Intensive Care, Karlstad Central Hospital, Karlstad; and the
Örebro University Hospital, Örebro, Sweden.

Address correspondence to: Dr. Magnus Wattwil, Department of Anesthesiology and Intensive Care, Örebro University Hospital, 701 85 Örebro, Sweden. Phone: +46 19 602 10 00; Fax: +46 19 12 74 79; E-mail: magnus.wattwil{at}orebroll.se

Purpose: The mechanism of the antiemetic actions of corticosteroids is not known. The purpose of this study was to evaluate if betamethasone can prevent nausea, vomiting or increase of vasopressin induced by apomorphine. Metoclopramide, a dopamine antagonist, was used as a control substance.

Methods: Ten healthy volunteers were studied on three occasions. In a randomized order they were allocated to receive pretreatment with betamethasone 8 mg iv, metoclopramide 10 mg iv, and normal saline 2 mL as placebo on the three different occasions, 15 min before the administration of apomorphine 30 µg·kg^–1 sc. After administration of apomorphine, episodes of vomiting were recorded, and the intensity of nausea was estimated by the subject on a visual analogue scale (VAS 0–10 cm). Blood samples for analysis of plasma concentrations of vasopressin were analyzed.

Results: One volunteer decided to withdraw, as he experienced akathisia after receiving metoclopramide. During the first two hours after apomorphine, eight of nine volunteers vomited both after betamethasone and placebo. One volunteer did not vomit after betamethasone and placebo but he experienced nausea. None of the volunteers vomited after metoclopramide (P < 0.01 vs betamethasone and placebo). The maximum VAS for nausea was significantly higher after betamethasone and placebo compared to metoclopramide (P < 0.01). The vasopressin levels increased after betamethasone and placebo, but there was no increase in any volunteer after pretreatment with metoclopramide.

Conclusion: This study demonstrates that betamethasone does not prevent nausea, vomiting and increase of vasopressin induced by apomorphine, whereas metoclopramide prevents apomorphine-induced emesis. Our work suggests that betamethasone does not have dopamine-antagonistic effects.