HYPERALGESIA MEDIATED BY SPINAL GLUTAMATE OR SUBSTANCE-P RECEPTOR BLOCKED BY SPINAL CYCLOOXYGENASE INHIBITION
HYPERALGESIA MEDIATED BY SPINAL GLUTAMATE OR SUBSTANCE-P RECEPTOR BLOCKED BY SPINAL CYCLOOXYGENASE INHIBITION
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DOI：
10.1126/science.1381521
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发表时间：
1992-08-28
期刊：
影响因子：
56.9
通讯作者：
YAKSH, TL
中科院分区：
文献类型：
--
作者：
MALMBERG, AB;YAKSH, TL
通过非甾体抗炎药（NSAID）抑制外周环氧合酶通常被认为是这些药物产生选择性减轻疼痛（镇痛）的主要机制。现在显示NSAID通过阻断由脊髓谷氨酸盐和P物质受体的激活诱导的对疼痛的过度敏感性（痛觉过敏）来发挥直接的脊髓作用。这些发现表明，NSAID的镇痛作用可以从其抗炎作用中分离出来。因此，脊髓前列腺素类对于脊髓水平疼痛信息的增强处理至关重要。
Inhibition of cyclooxygenase by nonsteroidal anti-inflammatory drugs (NSAIDs) in the periphery is commonly accepted as the primary mechanism by which these agents produce a selective attenuation of pain (analgesia). NSAIDs are now shown to exert a direct spinal action by blocking the excessive sensitivity to pain (hyperalgesia) induced by the activation of spinal glutamate and substance P receptors. These findings demonstrate that the analgesic effects of NSAIDs can be dissociated from their anti-inflammatory actions. Spinal prostanoids are thus critical for the augmented processing of pain information at the spinal level.