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没有证据表明恐惧引起的阿片类药物介导的镇痛作用。

No evidence for opioid-mediated analgesia induced by phobic fear.

作者信息

Janssen S A, Arntz A

机构信息

Department of Medical Psychology, Maastricht University, The Netherlands.

出版信息

Behav Res Ther. 1997 Sep;35(9):823-30. doi: 10.1016/s0005-7967(97)00046-6.

DOI:10.1016/s0005-7967(97)00046-6
PMID:9299802
Abstract

The influence of anxiety on acute pain sensation was investigated, studying the relative contribution of endogenous opioids and attentional mechanisms. Thirty-six spider phobics received mildly painful electrical stimulation, while anxiety and focus of attention were manipulated within subjects. The opioid antagonist naloxone or placebo was administered between subjects to examine an analgesia owing to anxiety-induced endorphinergic activity. In contrast to earlier findings, attention towards pain failed to increase pain as opposed to distraction from pain, probably owing to a less effective attention manipulation. Furthermore, despite high levels of anxiety, subjective pain ratings were not influenced by anxiety, although heart rate responses were slightly inhibited. Accordingly, there was no increase in subjective or physiological pain responses as a result of naloxone, nor did beta-endorphin plasma levels rise during anxiety. The results suggest that phobic anxiety does not induce an opioid-mediated analgesia. Curiously, naloxone itself effected a dose-dependent analgesia compared to placebo during both high and low anxiety, which is compatible with the assumption of agonist properties of naloxone in the absence of opioid activity.

摘要

研究了焦虑对急性疼痛感觉的影响,探讨内源性阿片类物质和注意力机制的相对作用。36名蜘蛛恐惧症患者接受轻度疼痛的电刺激,同时在受试者内部对焦虑和注意力焦点进行操控。在受试者之间给予阿片类拮抗剂纳洛酮或安慰剂,以检验因焦虑诱导的内啡肽能活动所致的镇痛作用。与早期研究结果相反,对疼痛的关注与分散对疼痛的注意力相比,未能增加疼痛,这可能是由于注意力操控效果欠佳。此外,尽管焦虑程度很高,但主观疼痛评分并未受到焦虑的影响,尽管心率反应略有抑制。因此,纳洛酮并未导致主观或生理疼痛反应增加,焦虑期间血浆β-内啡肽水平也未升高。结果表明,恐惧性焦虑不会诱导阿片类介导的镇痛作用。奇怪的是,与安慰剂相比,纳洛酮在高焦虑和低焦虑状态下均产生剂量依赖性镇痛作用,这与在无阿片类活性时纳洛酮具有激动剂特性的假设相符。

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