RESULTS:Pain increased in all groups, but there were significantly lower pain ratings in the Placebo group at 15 minutes after the injection, compared with the other two groups. Cortisol increased in all groups, but mostly so in the Nocebo group. Circulating beta-endorphin increased in all groups. Pain-ratings were not correlated with beta-endorphins or cortisol.

CONCLUSIONS:A placebo response, ie, a reduced pain level, was seen in the Placebo group at 15 minutes after the injection. The placebo response was not related to stress or to beta-endorphin. Expectation of a pain increase in the Nocebo group led to an increase in cortisol, but the expectation of pain increase and the resultant cortisol increase had no effect on pain.

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OBJECTIVE:The experiment tested whether the placebo and nocebo responses could be mediated via modulation of stress.

METHODS:Ischemic pain was induced in healthy volunteers (N = 59). When pain reached "7" on a 10-point scale, two groups of subjects received information that a pain relieving (the Placebo group) or a pain increasing (the Nocebo group) substance was injected. All injections contained physiological saline. A third group received no information and no injection (the Natural History group). Pain ratings and blood samples for analysis of cortisol and beta-endorphin were obtained every 5 minutes after pain equal to seven until the experiment was terminated.

RESULTS:Pain increased in all groups, but there were significantly lower pain ratings in the Placebo group at 15 minutes after the injection, compared with the other two groups. Cortisol increased in all groups, but mostly so in the Nocebo group. Circulating beta-endorphin increased in all groups. Pain-ratings were not correlated with beta-endorphins or cortisol.

CONCLUSIONS:A placebo response, ie, a reduced pain level, was seen in the Placebo group at 15 minutes after the injection. The placebo response was not related to stress or to beta-endorphin. Expectation of a pain increase in the Nocebo group led to an increase in cortisol, but the expectation of pain increase and the resultant cortisol increase had no effect on pain.

译文

目的:该实验测试了安慰剂和Nocebo反应是否可以通过调节压力来介导。

方法:健康志愿者诱发缺血性疼痛(N = 59)。当疼痛以10分制达到“ 7”时,两组受试者收到的信息是注射了缓解疼痛的药物(安慰剂组)或增加疼痛的药物(Nocebo组)。所有注射均含有生理盐水。第三组没有收到任何信息,也没有注射(自然史组)。疼痛等于7次后每5分钟获得疼痛评分和血液样本,用于分析皮质醇和β-内啡肽,直到实验终止。

结果:所有组的疼痛均增加,但与其他两组相比,安慰剂组在注射后15分钟时的疼痛评级显着降低。皮质醇在所有组中均增加,但在Nocebo组中大部分如此。循环中的β-内啡肽在所有组中均增加。疼痛评分与β-内啡肽或皮质醇无关。

结论:安慰剂组在15分钟后出现安慰剂反应,即疼痛程度减轻。注射。安慰剂反应与压力或β-内啡肽无关。 Nocebo组预期疼痛会导致皮质醇增加,但是预期疼痛增加以及随之而来的皮质醇升高对疼痛没有影响。

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