Seifert E, Schadel A, Prohaska P
Poliklinik fr Phoniatrie und Pädaudiologie, Westfälische Wilhelms-Universität Münster.
Laryngorhinootologie. 1994 Jun;73(6):342-5. doi: 10.1055/s-2007-997144.
Antidromic electrical stimulation of sensory nerves produces vascular hyperpermeability, plasma protein extravasation and oedema. The initial phase of this inflammatory reaction is induced by the release of the neuropeptides CGRP, SP and NKA; the later phase is induced by mast cells. In previous investigations we were able to show that the facial nerve of the rat contains CGRP, SP and NKA as well as mast cells. The same mechanism--increased vascular permeability--plasma extravasation--oedema--is thought to be part of the pathogenesis of Bell's palsy. Hence, we tried to produce neurogenic inflammations in the facial nerves of six adult Wistar rats. To assess plasma extravasation we used Evans blue, a dye which binds to serum albumin, according to the method described by Brokaw and White (1992). Having cut the facial nerve distal of the stylomastoid foramen we induced a neurogenic inflammation by the application of an electrical stimulus to the distal part of the nerve. In comparison to the contralateral, non-stimulated side, we recognized that the inflammatory reactions were limited to the area of the skin innervated by the posterior auricular nerve. So far, we can transfer this "neurogenic inflammation model" the well-known relationship between nerves and inflammatory reactions to this limited area innervated by the facial nerve.
感觉神经的逆向电刺激会导致血管通透性增加、血浆蛋白外渗和水肿。这种炎症反应的初始阶段是由神经肽降钙素基因相关肽(CGRP)、P物质(SP)和神经激肽A(NKA)的释放所诱导的;后期阶段则由肥大细胞诱导。在先前的研究中,我们能够证明大鼠的面神经含有CGRP、SP、NKA以及肥大细胞。相同的机制——血管通透性增加——血浆外渗——水肿——被认为是贝尔麻痹发病机制的一部分。因此,我们试图在六只成年Wistar大鼠的面神经中引发神经源性炎症。根据Brokaw和White(1992年)描述的方法,我们使用伊文思蓝(一种与血清白蛋白结合的染料)来评估血浆外渗情况。在切断茎乳孔远端的面神经后,我们通过对神经远端施加电刺激来引发神经源性炎症。与对侧未受刺激的一侧相比,我们认识到炎症反应局限于耳后神经支配的皮肤区域。到目前为止,我们可以将这种“神经源性炎症模型”——神经与炎症反应之间的众所周知的关系——应用到面神经支配的这个有限区域。