目的观察光化学法诱导猫脊髓损伤后的神经行为学、运动诱发电位及形态学改变,为研究脊髓损伤后神经再生与功能重建建立动物模型。方法将15只猫根据冷光源照射时间不同随机分为40min组、60min组和80min组。手术暴露脊髓后,用35mg/kg体重的玫瑰红静脉注射,联合应用强度为3000klx的冷光源照射T13脊髓节段。术后21d内连续观察动物神经行为学改变;于术后第21天检测动物的运动诱发电位,并与术前结果比较;取材观察动物脊髓组织形态学改变。结果3组动物在手术后21d内的神经行为学评分结果显示,损伤后动物下肢功能神经行为学评分降低,损伤程度与光照时间成正比。60min组和80min组动物损伤后运动诱发电位波形消失。3组动物的脊髓都有明显的缺血性坏死改变。结论光化学法可诱导猫脊髓内产生微血栓,从而使组织发生缺血性坏死。冷光源照射60min、80min的动物双下肢运动功能明显受损,与其病理学改变和电生理学改变相符,用这种方法制作不完全脊髓损伤模型稳定可靠。
Objective To explore the potential of creating a cat model of spinal cord infarction initiated by a photochemical reaction in terms of the neuroethology, motor evoked potential, and morphological outcomes. Methods Fifteen cats were divided into three groups at random. T13 in the spinal cord was photochemically irradiated for 40 rain, 60 rain or 80 rain in different groups. A photochemically-induced infarction was produced by intravenous in- jection of rose Bengal (35 mg/kg) combined with immediate cold light irradiation (3000 klx) of the spinal cord. Neuroethology changes were observed every day after the surgery for 21 days, and morphological changes were examined at day 21 , before which the motor evoked potential was examined and compared with measurements taken before injury. Results The spinal cord infarctions induced by intravenous injection of rose Bengal plus cold light irradiation for 40 min were stable by day 8, while the other two groups were stable by day 12. The size of the infarction area in the spinal cord was stable, while the neuroethology, electrophysiological and histopathological changes in the cats were significant. Conclusions All of the cats demonstrated decreased functional mobility after photochemically induced thrombosis of the spinal cord, with corresponding pathomorphological and electrophysiologic changes. The model of infarction was stable and reliable.