Devor M, White D M, Goetzl E J, Levine J D
Department of Zoology, Hebrew University of Jerusalem, Israel.
Neuroreport. 1992 Jan;3(1):21-4. doi: 10.1097/00001756-199201000-00005.
Normal nociceptors are sensitized by hyperalgesic mediators such as eicosanoids and tachykinins. The possibility that these mediators contribute to hyperalgesic pain associated with neural injury was investigated by examining their effects on the excitability of injured afferent nerve endings. In amounts that sensitize normal nociceptors and are hyperalgesic in normal skin, the eicosanoids prostaglandin I2 (PGI2), and 8(R),15(S)-dihydroxyicosatetraenoic acid (8(R),15(S)-diHETE) both excited some C-fibers in chronic neuromas of rat sciatic nerve. In contrast, the selective tachykinin-receptor agonists septide and senktide did not excite C-fibers. None of the mediators affected A-fibers. We conclude that PGI2 and 8(R),15(S)-diHETE may contribute to post-injury pain and hyperalgesia by an action on injured afferent endings.
正常伤害感受器会被类花生酸和速激肽等痛觉过敏介质致敏。通过研究这些介质对受损传入神经末梢兴奋性的影响,来探究它们是否会导致与神经损伤相关的痛觉过敏疼痛。类花生酸前列腺素I2(PGI2)和8(R),15(S)-二羟基二十碳四烯酸(8(R),15(S)-diHETE)在能使正常伤害感受器致敏并在正常皮肤中产生痛觉过敏的剂量下,均可兴奋大鼠坐骨神经慢性神经瘤中的一些C纤维。相比之下,选择性速激肽受体激动剂septide和senktide不会兴奋C纤维。这些介质均不会影响A纤维。我们得出结论,PGI2和8(R),15(S)-diHETE可能通过作用于受损传入末梢而导致损伤后疼痛和痛觉过敏。