Hahn A F, Feasby T E, Gilbert J J
Acta Neuropathol. 1985;68(2):101-9. doi: 10.1007/BF00688630.
The integrity of the blood-nerve barrier (BNB) was studied during the development of experimental allergic neuritis (EAN). Lewis rats immunized with bovine nerve or myelin plus complete Freund's adjuvant developed histological lesions of EAN in nerve roots by 10-12 days and in sciatic nerves by 12-14 days. Evans blue-albumin (EBA) and horseradish peroxidase (HRP) were injected i.v. 1 h prior to killing on days 6-18. Perivascular and diffuse endoneurial leakage of the tracers was seen in nerve roots by 10-12 days post immunization (p.i.) and in sciatic nerves by 12-14 days. This coincided with the appearance of endoneurial infiltration with inflammatory cells and endoneurial proteinaceous edema at a time when Schwann cell and myelin changes were still minimal. Therefore, an alteration in BNB permeability occurs early in EAN, coincident with inflammatory cell infiltration. This could be an expression of delayed hypersensitivity, yet it would also facilitate the entry of anti-myelin antibodies into the endoneurium where they could initiate demyelination.
在实验性变应性神经炎（EAN）发展过程中，对血-神经屏障（BNB）的完整性进行了研究。用牛神经或髓磷脂加完全弗氏佐剂免疫的Lewis大鼠，在10-12天时神经根出现EAN的组织学病变，在12-14天时坐骨神经出现病变。在第6-18天处死前1小时静脉注射伊文思蓝-白蛋白（EBA）和辣根过氧化物酶（HRP）。免疫后10-12天在神经根可见示踪剂的血管周围和弥漫性神经内膜渗漏，12-14天在坐骨神经可见。这与神经内膜出现炎性细胞浸润和神经内膜蛋白性水肿同时发生，此时施万细胞和髓鞘变化仍很轻微。因此，EAN早期血-神经屏障通透性发生改变，与炎性细胞浸润同时出现。这可能是迟发型超敏反应的一种表现，但它也会促进抗髓鞘抗体进入神经内膜，在那里它们可引发脱髓鞘。
