Axelsson Patric, Thörn Sven-Egron, Lövqvist Asa, Wattwil Lisbeth, Wattwil Magnus
Department of Anesthesiology, Karlstad Central Hospital.
Can J Anaesth. 2006 Apr;53(4):370-4. doi: 10.1007/BF03022501.
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.
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 microg x kg(-1) s.c.. 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.
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.
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.
皮质类固醇的止吐作用机制尚不清楚。本研究的目的是评估倍他米松是否能预防阿扑吗啡诱导的恶心、呕吐或血管加压素升高。多巴胺拮抗剂甲氧氯普胺用作对照物质。
对10名健康志愿者进行了三次研究。他们以随机顺序在三种不同情况下分别接受以下预处理：静脉注射8毫克倍他米松、静脉注射10毫克甲氧氯普胺以及静脉注射2毫升生理盐水作为安慰剂，均在皮下注射30微克/千克阿扑吗啡前15分钟进行。注射阿扑吗啡后，记录呕吐发作情况，并由受试者通过视觉模拟量表（VAS 0 - 10厘米）评估恶心程度。采集血样分析血浆血管加压素浓度。
一名志愿者在接受甲氧氯普胺后出现静坐不能，决定退出研究。在注射阿扑吗啡后的头两个小时内，9名志愿者中有8名在接受倍他米松和安慰剂后均出现呕吐。一名志愿者在接受倍他米松和安慰剂后未呕吐，但出现了恶心。所有志愿者在接受甲氧氯普胺后均未呕吐（与倍他米松和安慰剂相比，P < 0.01）。与甲氧氯普胺相比，倍他米松和安慰剂后恶心的最大VAS显著更高（P < 0.01）。倍他米松和安慰剂后血管加压素水平升高，但接受甲氧氯普胺预处理的志愿者中无一例升高。
本研究表明，倍他米松不能预防阿扑吗啡诱导的恶心、呕吐和血管加压素升高，而甲氧氯普胺可预防阿扑吗啡诱导的呕吐。我们的研究表明倍他米松不具有多巴胺拮抗作用。
