Frid M, Singer G
Psychopharmacology (Berl). 1979 Jun 21;63(3):211-5. doi: 10.1007/BF00433552.
In this study the hypothesis that hypnotic analgesia under conditions of stress is mediated through a neurochemical mechanism involving the release of opioid peptides in the CNS was investigated. Ten highly hypnotizable subjects participated in a 2 x 2 factorial design, which involved hypnotic analgesia, stress and double blind administration of naloxone (an opiate antagonist) or placebo. Analysis of post-hypnosis results indicates that hypnotic analgesia was significantly reversed by the interactive effects of stress and naloxone. It is inferred that stress may be the common psychological denominator of the various analgesic methods which effectively engage this endogenous pain inhibitory system. Additional analyses of anxiety measures reveals no significant association between trait and state anxiety, but significant relationships between state anxiety and time tolerance to ischemic pain. These results suggest that anxiety remains a definitional problem and that previous conceptualizations may not have satisfactorily explained the affect's adaptive function.
在本研究中,对以下假设进行了调查:应激条件下的催眠镇痛是通过一种神经化学机制介导的,该机制涉及中枢神经系统中阿片肽的释放。十名高度可催眠的受试者参与了一项2×2析因设计,其中涉及催眠镇痛、应激以及纳洛酮(一种阿片拮抗剂)或安慰剂的双盲给药。催眠后结果分析表明,应激和纳洛酮的交互作用显著逆转了催眠镇痛效果。据推断,应激可能是有效激活这种内源性疼痛抑制系统的各种镇痛方法的共同心理因素。对焦虑测量的进一步分析表明,特质焦虑与状态焦虑之间无显著关联,但状态焦虑与缺血性疼痛的时间耐受性之间存在显著关系。这些结果表明,焦虑仍然是一个定义问题,并且先前的概念化可能未能令人满意地解释这种影响的适应性功能。