The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1095 NW 14th Terrace (R-48), Miami, FL 33136, USA.
Neuropharmacology. 2010 Mar-Apr;58(4-5):758-66. doi: 10.1016/j.neuropharm.2009.12.010. Epub 2009 Dec 24.
Pre-clinical evidence demonstrates that neuropathic spinal cord injury (SCI) pain is maintained by a number of neurobiological mechanisms, suggesting that treatments directed at several pain-related targets may be more advantageous compared to a treatment focused on a single target. The current study evaluated the efficacy of the non-opiate analgesic acetaminophen, which has several putative analgesic mechanisms, combined with analgesic drugs used to treat neuropathic pain in a rat model of below-level neuropathic SCI pain. Following an acute compression of the mid-thoracic spinal cord, rats exhibited robust hind paw hypersensitivity to innocuous mechanical stimulation. Fifty percent antinociceptive doses of gabapentin, morphine, tramadol or memantine were combined with an ineffective dose of acetaminophen; acetaminophen alone was not antinociceptive. The combination of acetaminophen with either tramadol or memantine resulted in an additive antinociceptive effect. Acetaminophen combined with either morphine or gabapentin, however, resulted in supra-additive (synergistic) efficacy. One of the analgesic mechanisms of acetaminophen is inhibiting the uptake of endocannabinoids from the extracellular space. Pre-treatment with AM251, a cannabinoid-1 receptor (CB1) antagonist, significantly diminished the antinociceptive effect of the acetaminophen + gabapentin combination. Pre-treatment with AM630, a cannabinoid-2 receptor (CB2) antagonist, did not have an effect on this combination. By contrast, both AM251 and AM630 reduced the efficacy of the acetaminophen + morphine combination. None of the active drugs alone were affected by either CB receptor antagonist. The results imply that modulation of the endocannabinoid system in addition to other mechanisms mediate the synergistic antinociceptive effects of acetaminophen combinations. Despite the presence of a cannabinoid mechanism, synergism was not present in all acetaminophen combinations. The combination of currently available drugs may be an appropriate option in ameliorating neuropathic SCI pain if single drug therapy is ineffective.
临床前证据表明,神经性脊髓损伤 (SCI) 疼痛是由多种神经生物学机制维持的,这表明针对多个与疼痛相关的靶点的治疗可能比针对单一靶点的治疗更有利。本研究评估了非阿片类镇痛药对乙酰氨基酚的疗效,对乙酰氨基酚具有几种假定的镇痛机制,与用于治疗神经性疼痛的药物联合用于治疗神经性 SCI 疼痛的大鼠模型。在急性压迫中胸段脊髓后,大鼠表现出对无害机械刺激的强烈后爪过敏。加巴喷丁、吗啡、曲马多或美金刚的 50%镇痛剂量与无效剂量的对乙酰氨基酚结合;单独使用对乙酰氨基酚没有镇痛作用。对乙酰氨基酚与曲马多或美金刚联合使用可产生相加的镇痛作用。然而,对乙酰氨基酚与吗啡或加巴喷丁联合使用会产生超相加(协同)疗效。对乙酰氨基酚的一种镇痛机制是抑制细胞外空间内内源性大麻素的摄取。预先用 AM251(大麻素 1 型受体 (CB1) 拮抗剂)处理可显著降低对乙酰氨基酚+加巴喷丁联合用药的镇痛作用。预先用 AM630(大麻素 2 型受体 (CB2) 拮抗剂)处理对这种联合用药没有影响。相反,AM251 和 AM630 均降低了对乙酰氨基酚+吗啡联合用药的疗效。单独使用的任何活性药物均不受任何 CB 受体拮抗剂的影响。结果表明,除其他机制外,内源性大麻素系统的调节介导了对乙酰氨基酚联合用药的协同镇痛作用。尽管存在大麻素机制,但并非所有对乙酰氨基酚联合用药都存在协同作用。如果单一药物治疗无效,当前可用药物的联合使用可能是改善神经性 SCI 疼痛的适当选择。