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首页> 外文期刊>Life sciences >Preemptive effects of intrathecal cyclooxygenase inhibitor or nitric oxide synthase inhibitor on thermal hypersensitivity following peripheral nerve injury
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Preemptive effects of intrathecal cyclooxygenase inhibitor or nitric oxide synthase inhibitor on thermal hypersensitivity following peripheral nerve injury

机译：鞘内环氧合酶抑制剂或一氧化氮合酶抑制剂对周围神经损伤后热超敏反应的先发作用

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The present study provides an important implication for the management of chronic neuropathic pain, focusing on prostaglandin (PG) and nitric oxide (NO) in the spinal cord. To determine if spinally administered cyclooxygenase (COX) inhibitor or nitric oxide synthase (NOS) inhibitor had preemptive analgesia on thermal hypersensitivity induced by chronic constrictive nerve injury, Sprague-Dawley rats were chronically implanted with an intrathecal (i.t.) catheter. The left sciatic nerve was loosely ligated with 2-mm polyethylene tubing to produce painful mononeuropathy. Animals received tenoxicam (7.5, 15 or 30 mumol/10 mul, i.t.), NS-398 (15 or 30 mumol), or L-NAME (30, 150 or 300 mumol) immediately before the nerve injury, followed by daily injection extending into the four postoperative days. The hindpaw was immersed into a hot (42degreesC, 44degreesC and 46degreesC) or cold (10degreesC) water bath. The paw immersion test revealed significant thermal hyperalgesia and allodynia 5 day after nerve injury in vehicle control animals. Tenoxicam (7.5, 15 or 30 mumol) or L-NAME (30, 150 or 300 mumol) dose-dependently attenuated hyperalgesia and allodynia. Equimolar dose of NS-398 (15 or 30 mumol) also diminished these nociceptive behaviors. Higher dose of either drug primarily produced longer duration of inhibition. The inhibitory effect of tenoxicam (30 mumol) on hyperalgesia was more effective than that of an equimolar dose of NS-398 or L-NAME. These results demonstrated that intrathecally administered COX inhibitor or NOS inhibitor provides preemptive analgesia on thermal hypersensitivity following chronic constrictive nerve injury in rats. (C) 2004 Elsevier Inc. All rights reserved.
机译：本研究为慢性神经性疼痛的治疗提供了重要的启示，重点是脊髓中的前列腺素（PG）和一氧化氮（NO）。为了确定脊髓施用的环氧合酶（COX）抑制剂或一氧化氮合酶（NOS）抑制剂对慢性收缩性神经损伤引起的热超敏反应具有先发镇痛作用，将Sprague-Dawley大鼠长期植入鞘内（i.t.）导管。将左坐骨神经与2毫米聚乙烯管松散结扎，以产生痛苦的单神经病。动物在神经损伤前立即接受替诺昔康（7.5、15或30摩尔mol / 10倍），NS-398（15或30摩尔）或L-NAME（30、150或300摩尔），然后每天注射一次进入术后四天。将后爪浸入热水（42℃，44℃和46℃）或冷水（10℃）中。爪浸入试验显示，在媒介物对照动物神经损伤后5天，有明显的热痛觉过敏和异常性疼痛。替诺昔康（7.5、15或30摩尔）或L-NAME（30、150或300摩尔）剂量依赖性地减轻痛觉过敏和异常性疼痛。等摩尔剂量的NS-398（15或30摩尔）也减少了这些伤害行为。任一种药物的较高剂量主要产生更长的抑制持续时间。替诺昔康（30摩尔）对痛觉过敏的抑制作用比等摩尔剂量的NS-398或L-NAME更为有效。这些结果证明鞘内施用的COX抑制剂或NOS抑制剂对大鼠慢性收缩性神经损伤后的热超敏反应提供先发性镇痛作用。 （C）2004 Elsevier Inc.保留所有权利。

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