Tissue injury and related mediators of pain exacerbation.
Tissue injury and related mediators of pain exacerbation.
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DOI：
10.2174/1570159x11311060003
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发表时间：
2013-12
影响因子：
5.3
通讯作者：
Sasaki M
中科院分区：
文献类型：
--
作者：
Amaya F;Izumi Y;Matsuda M;Sasaki M
组织损伤和炎症导致各种介质的释放，促进对机械、热和化学刺激的持续疼痛或疼痛超敏反应。前伤害性介质直接或间接激活初级传入神经元，增强伤害性信号向中枢神经系统的传递。外周源性介质对初级传入事件的激发，即所谓的“外周致敏”，是组织损伤相关疼痛的一个标志。损伤组织中合成的ATP、谷氨酸、激肽、细胞因子和营养因子等多种促伤害介质参与了外周致敏的发生。在本综述中，我们将讨论组织损伤后外周致敏的分子机制。
Tissue injury and inflammation result in release of various mediators that promote ongoing pain or pain hypersensitivity against mechanical, thermal and chemical stimuli. Pro-nociceptive mediators activate primary afferent neurons directly or indirectly to enhance nociceptive signal transmission to the central nervous system. Excitation of primary afferents by peripherally originating mediators, so-called “peripheral sensitization”, is a hallmark of tissue injury-related pain. Many kinds of pro-nociceptive mediators, including ATP, glutamate, kinins, cytokines and tropic factors, synthesized at the damaged tissue, contribute to the development of peripheral sensitization. In the present review we will discuss the molecular mechanisms of peripheral sensitization following tissue injury.