NALOXONE-REMIFENTALIL PAIN MODULATION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 抵消止痛是由伤害性刺激强度的微小下降引起的疼痛的不成比例的大幅下降。这种止痛现象可能代表了一种中枢介导的时间对比度增强机制。已知阿片机制自然发生在体内(Anderson等人，2002，Goldstein，1976，Basbaum和Fields，1978)。在某些身体状况下，这些药物起到减轻疼痛的作用。为了验证这些阿片机制部分支持抵消镇痛的假说，我们将评估志愿者静脉注射阿片类拮抗剂纳洛酮和阿片激动剂瑞芬太尼期间抵消镇痛的变化。本研究的总体目标是系统地描述抵消镇痛的神经生理学和神经药理学机制。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Offset analgesia is a disproportionately large decrease in pain evoked by small decreases in noxious stimulus intensity. This analgesic phenomenon may represent a centrally mediated temporal contrast enhancement mechanism. Opioid mechanisms are known to naturally occur in the body (Anderson et al., 2002, Goldstein, 1976, Basbaum and Fields, 1978). These act to diminish pain in certain bodily situations. In order to test the hypothesis that offset analgesia is partially supported by these opioid mechanisms, changes in offset analgesia will be assessed in volunteers during intravenous administration of the opioid antagonist naloxone and of the opioid agonist remifentanil. The overall objectives of this study are to systematically delineate the neurophysiological and neuropharmacological mechanisms that subserve offset analgesia.