Green P G, Luo J, Heller P H, Levine J D
Department of Medicine, University of California, San Francisco 94143.
Neuroscience. 1993 Aug;55(4):1037-43. doi: 10.1016/0306-4522(93)90317-9.
This study provides significant new evidence substantiating a role of the postganglionic sympathetic neuron in plasma extravasation in the knee-joint of the rat. Increased plasma extravasation produced by the potent inflammatory mediator bradykinin was mimicked by 6-hydroxydopamine, a selective stimulator of sympathetic fibers. Various treatments (chemical sympathectomy, co-perfusion with the local anesthetic lidocaine, or co-perfusion with depolarizing concentrations of potassium) similarly modulated plasma extravasation induced by both bradykinin and 6-hydroxydopamine, but not that produced by platelet activating factor. We also showed that bradykinin is able to release norepinephrine in the knee-joint, indicating action on the sympathetic postganglionic neuron. In summary, these experiments provide substantial additional evidence supporting a significant contribution of the sympathetic post-ganglionic neuron terminal to inflammatory plasma extravasation.
本研究提供了重要的新证据,证实了节后交感神经元在大鼠膝关节血浆外渗中的作用。强效炎症介质缓激肽引起的血浆外渗增加,可被交感神经纤维的选择性刺激剂6-羟基多巴胺模拟。各种处理(化学去交感神经、与局部麻醉剂利多卡因共同灌注或与去极化浓度的钾共同灌注)同样调节了缓激肽和6-羟基多巴胺诱导的血浆外渗,但对血小板活化因子引起的血浆外渗没有影响。我们还表明,缓激肽能够在膝关节释放去甲肾上腺素,表明其对交感节后神经元有作用。总之,这些实验提供了大量额外证据,支持交感节后神经元末梢对炎症性血浆外渗有重要贡献。