Inducing placebo respiratory depressant responses in humans via opioid receptors
Inducing placebo respiratory depressant responses in humans via opioid receptors
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DOI：
10.1046/j.1460-9568.1999.00465.x
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发表时间：
1999-02-01
影响因子：
3.4
通讯作者：
Maggi, G
中科院分区：
文献类型：
--
作者：
Benedetti, F;Amanzio, M;Maggi, G
几条证据表明，安慰剂通过激活内源性阿片系统产生镇痛作用。最近，我们发现，安慰剂也可能产生呼吸抑制反应，一个典型的副作用的麻醉剂，当一个受试者有呼吸抑制的经验，在麻醉治疗过程中，在本研究中，我们报告，安慰剂呼吸抑制可以诱导后，重复给药的部分阿片受体激动剂丁丙诺啡。丁丙诺啡预处理引起的安慰剂呼吸抑制效应被10 mg剂量的纳洛酮完全阻断，表明其由内源性阿片类药物介导。这些发现表明，安慰剂通过激活阿片受体，不仅作用于疼痛机制，而且作用于呼吸中枢，从而模仿麻醉剂的典型副作用。此外，我们使用的实验程序没有产生任何呼吸抑制的预期，同样，受试者没有注意到任何呼吸不适的迹象。因此，本研究中引起的安慰剂呼吸抑制不能根据认知或动机机制来解释。相反，它似乎是一个序列效应，由于学习，从而表明一个条件反射机制介导的内源性阿片类药物。
Several lines of evidence indicate that placebos produce analgesia through the activation of endogenous opioid systems. Recently, we showed that placebos may also produce respiratory depressant responses, a typical side-effect of narcotics, when a subject had a prior experience of respiratory depression in the course of narcotic treatment, in the present study, we report that the placebo respiratory depression can be induced after repeated administrations of the partial opioid agonist buprenorphine. The placebo respiratory depressant effect that resulted from the buprenorphine conditioning was completely blocked by a dose of 10 mg of naloxone, indicating that it was mediated by endogenous opioids. These findings show that placebos act, via the activation of opioid receptors, not only on pain mechanisms but on the respiratory centres as well, thus mimicking a typical side-effect of narcotics. In addition, the experimental procedure we used did not produce any expectation of respiratory depression and, similarly, the subjects did not notice any sign of respiratory discomfort. Thus, the placebo respiratory depression elicited in the present study cannot be explained on the basis of cognitive or motivational mechanisms. Rather, it appears to be a sequence effect due to learning, thus suggesting a conditioning mechanism mediated by endogenous opioids.