Watson B D, Prado R, Dietrich W D, Ginsberg M D, Green B A
Brain Res. 1986 Mar 5;367(1-2):296-300. doi: 10.1016/0006-8993(86)91606-9.
We have developed in the rat a minimally invasive model of reproducible spinal cord injury initiated photochemically. With the exposed spinal column intact, 560 nm irradiation of the translucent dorsal surface induces excitation of the systemically injected dye, rose Bengal, in the spinal cord microvasculature. The resultant photochemical reaction leads to vascular stasis. Histopathological changes at 7 days include hemorrhagic necrosis of the central gray matter, edematous pale-staining white matter tracts and vascular congestion. At the level of cord irradiation (T8) the entire cord thickness is necrosed except for the periphery of the anterior funiculus. Voluntary motor function is consistently lost in the subacute phase of injury.
我们在大鼠身上建立了一种微创的、可重复的光化学诱导脊髓损伤模型。在完整暴露的脊柱情况下,对半透明的背侧表面进行560纳米的照射,可诱导全身注射的染料孟加拉玫瑰红在脊髓微血管系统中被激发。由此产生的光化学反应导致血管淤滞。7天时的组织病理学变化包括中央灰质的出血性坏死、水肿性淡染的白质束和血管充血。在脊髓照射水平(T8),除前索周边外,整个脊髓厚度均发生坏死。在损伤的亚急性期,自主运动功能持续丧失。