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

Abstract

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. Objectif

What is nausea? A historical analysis of changing views

“…Often the stimulus used in these experiments was a moving visual field (Farmer et al, 2015; Koch, 1999; Sclocco et al, 2015; Sclocco et al, 2016), which is regularly (but erroneously) referred to as “vection.” Vection is an illusion of self-motion, and studies that utilize moving visual fields to induce motion sickness rarely attempt to validate if the stimulus evokes a perception of self-movement (Lawson et al, 2015). Although some experimental studies in humans used agents such as apomorphine or ipecacuanha to induce nausea (Axelsson et al, 2006; Nussey et al, 1988; Proctor et al, 1978; Rowe et al, 1979), employing moving visual fields has two principal advantages: it is not necessary to administer agents that could produce extraneous side effects and the stimulus can be rapidly terminated at the subject’s request.…”

Betamethasone in prevention of postoperative nausea and vomiting following breast surgery

“…The antiemetic mechanism of action still remains unclear, but previous studies have excluded dopamine-and/or 5HT-3 antagonistic effects [17,18].…”

Apomorphine Is a Bimodal Modulator of TRPA1 Channels

“…In humans and in dogs, administration of apomorphine is accompanied by severe nausea and emesis (Lefebvre et al, 1981;Axelsson et al, 2006). In general, mechanisms by which drug-induced emesis can be triggered are diverse.…”