NEURAL MECHANISMS OF INFLAMMATION AND HYPERALGESIA

急性炎症的体液介质可分为以下几种 激活伤害性传入并产生疼痛(例如，缓激肽)，以及 那些使人敏感但不会激活伤害性感受器并产生 痛觉过敏(如E-型前列腺素)。然而，这种相关性很差 炎症介质浓度和炎症强度之间的关系 某些病理情况下的症状(如类风湿性关节炎) 阿司匹林类药物未能持续产生止痛 与炎症相关的疼痛和痛觉过敏表明 其他调解人也参与了这些症状的产生。我们建议 研究白三烯的贡献，一类新发现的白三烯 花生四烯酸代谢物，其合成不受 阿司匹林类药物，与疼痛和痛觉过敏有关 炎症，以期改善人类的症状管理。在……里面 初步实验我们已经找到证据证明 白三烯-B4受体介导的痛敏效应。

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.