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脑阿片受体在高压氧治疗坐骨神经挤压损伤诱导的神经病理性疼痛大鼠中的抗痛觉过敏作用中的作用。

Involvement of brain opioid receptors in the anti-allodynic effect of hyperbaric oxygen in rats with sciatic nerve crush-induced neuropathic pain.

机构信息

Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Pullman, WA, USA.

出版信息

Brain Res. 2013 Nov 6;1537:111-6. doi: 10.1016/j.brainres.2013.08.050. Epub 2013 Aug 30.

Abstract

Earlier research has demonstrated that hyperbaric oxygen (HBO2) can produce an antinociceptive effect in models of acute pain. Recent studies have revealed that HBO2 can produce pain relief in animal models of chronic pain as well. The purpose of the present investigation was to ascertain whether HBO2 treatment might suppress allodynia in rats with neuropathic pain and whether this effect might be blocked by the opioid antagonist naltrexone (NTX). Male Sprague Dawley rats were subjected to a sciatic nerve crush under anesthesia and mechanical thresholds were assessed using an electronic von Frey anesthesiometer. The time course of the HBO2-induced anti-allodynic effect in different treatment groups was plotted, and the area-under-the-curve (AUC) was determined for each group. Seven days after the nerve crush procedure, rats were treated with HBO2 at 3.5 atm absolute (ATA) for 60 min and exhibited an anti-allodynic effect, compared to nerve crush-only control rats. Twenty-four hours before HBO2 treatment, another group of rats was implanted with Alzet(®) osmotic minipumps that continuously released NTX into the lateral cerebral ventricle for 7 days. These NTX-infused, HBO2-treated rats exhibited an allodynic response comparable to that exhibited by rats receiving nerve crush only. Analysis of the AUC data showed that HBO2 significantly reduced the nerve crush-induced allodynia; this anti-allodynic effect of HBO2 was reversed by NTX. These results implicate opioid receptors in the pain relief induced by HBO2.

摘要

早期研究表明,高压氧(HBO2)可在急性疼痛模型中产生镇痛作用。最近的研究表明,HBO2 也可以在慢性疼痛的动物模型中产生缓解疼痛的效果。本研究的目的是确定 HBO2 治疗是否可以抑制神经病理性疼痛大鼠的触诱发痛,以及这种效应是否可以被阿片受体拮抗剂纳曲酮(NTX)阻断。雄性 Sprague Dawley 大鼠在麻醉下接受坐骨神经挤压,并使用电子 von Frey 测痛仪评估机械阈值。绘制不同治疗组中 HBO2 诱导的抗触诱发痛作用的时间过程,并确定每组的曲线下面积(AUC)。在神经挤压手术后 7 天,大鼠接受 3.5 绝对大气压(ATA)的 HBO2 治疗 60 分钟,与仅接受神经挤压的对照组大鼠相比,表现出抗触诱发痛作用。在 HBO2 治疗前 24 小时,另一组大鼠被植入 Alzet(®)渗透型迷你泵,该泵持续 7 天向侧脑室内释放 NTX。这些接受 NTX 输注和 HBO2 治疗的大鼠表现出与仅接受神经挤压的大鼠相似的触诱发痛反应。AUC 数据分析表明,HBO2 显著减轻了神经挤压引起的触诱发痛;HBO2 的这种抗触诱发痛作用被 NTX 逆转。这些结果表明阿片受体参与了 HBO2 诱导的疼痛缓解。

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