Yu W, Kauppila T, Hultenby K, Persson J K, Xu X J, Wiesenfeld-Hallin Z
Karolinska Institutet, Department of Medical Laboratory Sciences and Technology, Huddinge University Hospital, Sweden.
J Peripher Nerv Syst. 2000 Dec;5(4):209-17. doi: 10.1046/j.1529-8027.2000.00024.x.
Lesion of presumably ischemic origin of the rat sciatic nerve was induced photochemically by laser irradiation combined with systemic administration of a photosensitizing organic dye, erythrosin B. We have studied the pathologic features of the nerve after the photochemical insult with light- and electronmicroscopy and related them to behavioral signs of neuropathic pain. At the irradiated nerve site, occlusion of blood vessels was seen and the vessels were packed with aggregated thrombocytes, fibrins and deformed erythrocytes, supporting the notion that photochemical reaction caused intraneural ischemia. The degree of the nerve injury at the center of irradiation was related to the duration of the laser exposure. Brief irradiation (30 seconds) only caused identifiable injury to myelinated fibers, whereas longer irradiation (2 minutes) caused greater injury to myelinated and unmyelinated fibers, characterized by extensive axonal degeneration and demyelination. The rats irradiated for 2 minutes, but not 30 seconds, exhibited neuropathic pain-like behaviors, expressed as mechanical and cold allodynia. The nerve injury was most severe 7 days after ischemia and regeneration of both myelinated and unmyelinated fibers was observed 3 months later. The nerve caudal to the irradiation exhibited Wallerian degeneration 7 days after the insult, whereas at 10 mm proximal to the irradiation the nerve was largely normal. It is thus concluded that photochemically induced intraneural ischemia caused injury to both myelinated and unmyelinated fibers, with myelinated fibers being more susceptible. However, the development of neuropathic pain-like behaviors may require injury to the unmyelinated fibers.
通过激光照射并全身给予光敏有机染料赤藓红B，以光化学方式诱导大鼠坐骨神经发生推测为缺血性的损伤。我们用光镜和电镜研究了光化学损伤后神经的病理特征，并将其与神经性疼痛的行为体征相关联。在照射的神经部位，可见血管闭塞，血管内充满聚集的血小板、纤维蛋白和变形的红细胞，这支持了光化学反应导致神经内缺血的观点。照射中心处的神经损伤程度与激光照射时间有关。短暂照射（30秒）仅对有髓纤维造成可识别的损伤，而较长时间照射（2分钟）对有髓和无髓纤维造成更大损伤，其特征为广泛的轴突退变和脱髓鞘。照射2分钟而非30秒的大鼠表现出神经性疼痛样行为，表现为机械性和冷觉异常性疼痛。缺血后7天神经损伤最为严重，3个月后观察到有髓和无髓纤维均再生。损伤后7天，照射部位尾侧的神经出现华勒氏变性，而在照射部位近端10毫米处，神经基本正常。因此得出结论，光化学诱导的神经内缺血对有髓和无髓纤维均造成损伤，其中有髓纤维更易受损。然而，神经性疼痛样行为的出现可能需要无髓纤维受到损伤。
