Grevert Priscilla, Albert Leonard H, Goldstein Avram
Addiction Research Foundation and Stanford University, Palo Alto, Calif. 94304 U.S.A.
Pain. 1983 Jun;16(2):129-143. doi: 10.1016/0304-3959(83)90203-8.
Thirty subjects were given a placebo (intravenous saline), which was described as a known pain killer, once a week for 3 consecutive weeks. Experimental ischemic arm pain was produced prior to the placebo and again 1 h later. In a double blind procedure, half of the subjects received 10 mg of naloxone after placebo; the remaining subjects received naloxone vehicle. In addition to the placebo session, there were control and naloxone sessions each week to determine the normal changes in pain and the effect of naloxone on the pain, respectively, when no placebo was given. Significant placebo-induced analgesia was demonstrated, and a group of consistent placebo responders was identified. Although naloxone alone had no effect on the experimental pain, naloxone diminished the analgesic effectiveness of the placebo, suggesting that endogenous opioids are involved in producing placebo-induced analgesia.
30名受试者连续3周每周接受一次安慰剂(静脉注射生理盐水),该安慰剂被描述为一种已知的止痛剂。在给予安慰剂之前以及1小时后再次诱发实验性缺血性手臂疼痛。在双盲程序中,一半受试者在接受安慰剂后接受10毫克纳洛酮;其余受试者接受纳洛酮溶媒。除了安慰剂疗程外,每周还有对照和纳洛酮疗程,分别用于确定在未给予安慰剂时疼痛的正常变化以及纳洛酮对疼痛的影响。证实了显著的安慰剂诱导镇痛作用,并识别出一组持续的安慰剂反应者。虽然单独使用纳洛酮对实验性疼痛没有影响,但纳洛酮降低了安慰剂的镇痛效果,这表明内源性阿片类物质参与了安慰剂诱导的镇痛作用。