Laboratório de Neurobiologia da Dor e Inflamação, Programa Pós-Graduação em Neurociências, Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Campus Universitário, Trindade, Florianópolis, Santa Catarina, Brazil.
Phys Ther. 2013 Mar;93(3):401-12. doi: 10.2522/ptj.20120226. Epub 2012 Oct 19.
Physical therapists frequently use joint mobilization therapy techniques to treat people with musculoskeletal dysfunction and pain. Several studies suggest that endogenous adenosine may act in an analgesic fashion in various pain states.
The purpose of this study was to investigate the contribution of the adenosinergic system on the antihyperalgesic effect of ankle joint mobilization (AJM).
This was a experimental study.
To test the hypothesis that the adrenosinergic system is involved in the antihyperalgesic effect of AJM, mice (25-35 g) submitted to plantar incision surgery were used as a model of acute postoperative pain. The mice were subjected to AJM for 9 minutes. Withdrawal frequency to mechanical stimuli was assessed 24 hours after plantar incision surgery and 30 minutes after AJM, adenosine, clonidine, or morphine treatments. The adenosinergic system was assessed by systemic (intraperitoneal), central (intrathecal), and peripheral (intraplantar) administration of caffeine. The participation of the A1 receptor was investigated using a selective adenosine A1 receptor subtype antagonist. In addition, previous data on the involvement of the serotonergic and noradrenergic systems in the antihyperalgesic effect of AJM were confirmed.
Ankle joint mobilization decreased mechanical hyperalgesia, and this effect was reversed by pretreatment of the animals with caffeine given by intraperitoneal, intraplantar, and intrathecal routes. In addition, intraplanar and intrathecal administrations of 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, a selective adenosine A1 subtype receptor antagonist) or systemic administration of yohimbine or ρ-chlorophenylalanine methyl ester hydrochloride (PCPA) blocked the antihyperalgesia induced by AJM.
The results are limited to animal models and cannot be generalized to acute pain in humans.
This study demonstrated the involvement of the adenosinergic system in the antihyperalgesic effect of AJM in a rodent model of pain and provides a possible mechanism basis for AJM-induced relief of acute pain.
物理治疗师经常使用关节松动治疗技术来治疗肌肉骨骼功能障碍和疼痛患者。有几项研究表明,内源性腺苷在各种疼痛状态下可能具有镇痛作用。
本研究旨在探讨嘌呤能系统对踝关节松动(AJM)的抗痛觉过敏作用的贡献。
这是一项实验研究。
为了验证嘌呤能系统参与 AJM 的抗痛觉过敏作用的假设,使用足底切口手术的小鼠(25-35g)作为急性术后疼痛模型。将小鼠进行 9 分钟的 AJM。在足底切口手术后 24 小时和 AJM、腺苷、可乐定或吗啡治疗后 30 分钟,评估对机械刺激的撤回频率。通过全身(腹腔内)、中枢(鞘内)和外周(足底内)给予咖啡因来评估嘌呤能系统。使用选择性腺苷 A1 受体亚型拮抗剂研究 A1 受体的参与。此外,还证实了先前关于 5-羟色胺能和去甲肾上腺素能系统参与 AJM 的抗痛觉过敏作用的数据。
踝关节松动可减轻机械性痛觉过敏,并且该作用可通过腹腔内、足底内和鞘内给予咖啡因预处理而逆转。此外,1,3-二丙基-8-环戊基黄嘌呤(DPCPX,一种选择性腺苷 A1 亚型受体拮抗剂)的足底内和鞘内给药或育亨宾或ρ-氯苯丙氨酸甲酯盐酸盐(PCPA)的全身给药阻断了 AJM 诱导的抗痛觉过敏。
结果仅限于动物模型,不能推广到人类的急性疼痛。
本研究表明嘌呤能系统参与了疼痛啮齿动物模型中 AJM 的抗痛觉过敏作用,并为 AJM 诱导缓解急性疼痛提供了可能的机制基础。