NEURAL MECHANISMS OF INFLAMMATION AND HYPERALGESIA

急性炎症的体液介质可分为 激活伤害性传入并产生疼痛（例如，缓激肽），和 那些致敏，但不激活伤害感受器，并产生 痛觉过敏（例如，E型野牡丹素）。 然而，相关性差 炎症介质的浓度和 某些病理状况下的症状（例如，类风湿性关节炎） 阿司匹林类药物不能持续产生镇痛作用 与炎症相关的疼痛和痛觉过敏表明， 其他介质参与产生这些症状。 我们建议 研究白三烯的贡献，一种新发现的 花生四烯酸代谢物，其合成不受 阿司匹林类药物，对疼痛和痛觉过敏相关的 炎症，以期改善人类的症状管理。 在 初步实验我们已经发现了 受体介导的白三烯-B4的痛觉过敏作用。

The humoral mediators of acute inflammation can be divided into those that activate nociceptive afferents and produce pain (e.g., bradykinin), and those that sensitize, but do not activate nociceptors and produce hyperalgesia (e.g., E-type prostaglandins). However, the poor correlation between the concentration of inflammatory mediators and intensity of symptoms in certain pathological conditions (e.g., rheumatoid arthritis) and the failure of the aspirin-like drugs to consistently produce analgesia for the pain and hyperalgesia associated with inflammation suggest that other mediators are involved in producing these symptoms. We propose to study the contribution of leukotrienes, a newly discovered class of arachidonic acid metabolites, whose synthesis is not inhibited by aspirin-like drugs, to the pain and hyperalgesia associated with inflammation with a view toward improving symptom management in humans. In preliminary experiments we have already found evidence for a receptor-mediated hyperalgesic effect of leukotriene-B4.