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血浆β-内啡肽水平揭示了内源性阿片样物质镇痛功能的哪些方面?

What do plasma beta-endorphin levels reveal about endogenous opioid analgesic function?

机构信息

Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA.

出版信息

Eur J Pain. 2012 Mar;16(3):370-80. doi: 10.1002/j.1532-2149.2011.00021.x. Epub 2011 Dec 19.

Abstract

Plasma levels of beta-endorphin (BE), an endogenous opioid analgesic, are often reported as they relate to acute and chronic pain outcomes. However, little is known about what resting plasma BE levels might reveal about functioning of the endogenous opioid antinociceptive system. This study directly examined associations between resting plasma BE and subsequent endogenous opioid analgesic responses to acute pain in 39 healthy controls and 37 individuals with chronic low back pain (LBP). Resting baseline levels of plasma BE were assessed. Next, participants received opioid blockade (8 mg naloxone i.v.) or placebo in a double-blind, randomized, crossover design. Participants then underwent two acute pain stimuli: finger pressure (FP) pain and ischaemic (ISC) forearm pain. Blockade effects (naloxone minus placebo pain ratings) were derived to index endogenous opioid analgesic function. In placebo condition analyses for both pain stimuli, higher resting BE levels were associated with subsequently greater reported pain intensity (p's < 0.05), with this effect occurring primarily in healthy controls (BE × Participant Type interactions, p's < 0.05). In blockade effect analyses across both pain tasks, higher resting plasma BE predicted less subsequent endogenous opioid analgesia (smaller blockade effects; p's < 0.05). For the ISC task, these links were significantly more prominent in LBP participants (BE × Participant Type Interactions, p's < 0.05). Results suggest that elevated resting plasma BE may be a potential biomarker for reduced endogenous opioid analgesic capacity, particularly among individuals with chronic pain. Potential clinical implications are discussed.

摘要

血浆β-内啡肽(BE)水平常被报道与急性和慢性疼痛结局有关,因为它是一种内源性阿片类镇痛物质。然而,关于静息血浆 BE 水平可能反映内源性阿片类镇痛系统功能的情况,人们知之甚少。本研究直接考察了 39 名健康对照者和 37 名慢性下背痛(LBP)患者的静息血浆 BE 与急性疼痛后内源性阿片类镇痛反应之间的相关性。评估了静息基础血浆 BE 水平。接下来,参与者以双盲、随机、交叉设计接受阿片受体拮抗剂(8mg 纳洛酮静脉注射)或安慰剂治疗。然后,参与者接受两种急性疼痛刺激:手指压迫(FP)疼痛和缺血(ISC)前臂疼痛。通过纳洛酮减去安慰剂的疼痛评分来获得阻滞效应,以评估内源性阿片类镇痛功能。在两种疼痛刺激的安慰剂条件分析中,较高的静息 BE 水平与随后报告的疼痛强度增加相关(p 值均 <0.05),这种效应主要发生在健康对照组中(BE×参与者类型交互作用,p 值均 <0.05)。在两种疼痛任务的阻滞效应分析中,较高的静息血浆 BE 预示着随后内源性阿片类镇痛作用减弱(较小的阻滞效应;p 值均 <0.05)。对于 ISC 任务,这些关联在 LBP 参与者中更为显著(BE×参与者类型交互作用,p 值均 <0.05)。结果表明,静息血浆 BE 升高可能是内源性阿片类镇痛能力降低的潜在生物标志物,尤其是在慢性疼痛患者中。讨论了潜在的临床意义。

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