痛觉过敏：综述
Hyperalgesic pain: a review.
作者信息
Levine J D, Taiwo Y O
机构信息
University of California, San Francisco.
出版信息
Anesth Prog. 1990 Mar-Jun;37(2-3):133-5.
Pain induced by a stimulus that is normally not painful is referred to as hyperalgesic pain. Inhibition of arachidonic acid metabolism and/or sympathectomy have been found to be effective treatment for this type of pain. We propose that the lowered pain threshold is induced by arachidonic acid metabolites produced in inflamed tissue or by sympathetic postganglionic neurons after nerve injury. The most extensively studied hyperalgesic mediators are prostaglandin E(2) (PGE(2)) and prostacyclin (PGI(2)), products of the cyclooxygenase pathway of arachidonic acid metabolism, whose production is inhibited by nonsteroidal antiinflammatory analgesics (NSAIAs). Recent studies, however, have demonstrated that products of the NSAIA-resistant lipoxygenase pathway of arachidonic acid metabolism are also hyperalgesic. Their production is inhibited by corticosteroids and current experimental agents.
由通常不会引起疼痛的刺激所诱发的疼痛被称为痛觉过敏疼痛。已发现抑制花生四烯酸代谢和/或交感神经切除术是治疗这类疼痛的有效方法。我们认为，疼痛阈值降低是由炎症组织中产生的花生四烯酸代谢产物或神经损伤后交感神经节后神经元引起的。研究最为广泛的痛觉过敏介质是前列腺素E(2)（PGE(2)）和前列环素（PGI(2)），它们是花生四烯酸代谢环氧化酶途径的产物，其生成可被非甾体抗炎镇痛药（NSAIA）抑制。然而，最近的研究表明，花生四烯酸代谢的NSAIA抗性脂氧合酶途径的产物也具有痛觉过敏作用。它们的生成可被皮质类固醇和当前的实验药物抑制。
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