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目的制作外伤性视神经病(traumatic optic neuropathy,TON)动物模型,观察其电生理及形态学改变,为指导临床救治提供参考。方法选择2只成年家猫进行视神经解剖观察;选择成年家猫30只,经上颌窦和鼻腔筛蝶窦双入路,用自制视神经管损伤器在内镜监视下损伤管内段视神经,建立 TON 模型。观察伤后瞳孔变化,监测损伤后1 h、1 d、3 d、1周、2周及4周时的图形翻转视觉诱发电位(pattern reversal visual evoked potential,PR-VEP)变化,并分别于损伤后1 d、3 d、1周、2周及4周处死动物,观察视神经组织的形态学改变。结果损伤后有8只猫患眼出现 Marcus-Gunn 黑朦强直性瞳孔,其余22只患眼直接和间接对光反射均不灵敏。VEP 各波:1 h、1 d、3 d、1周的 N_(75)P_(100)、P_(100)N_(145)振幅降低超过50%,N_(75)、P_(100)及 N_(145)潜伏期延长超过10 ms,2周以后的波形趋于一条直线。光镜下示视神经组织随时间推移而呈现空泡样变性,范围逐渐扩大,从伤后1 d 开始,视神经纤维束逐渐肿胀,纤维空泡变性;1周后空泡变性扩大为片状;至2周后出现大片空泡,并形成大空泡。电镜下示伤后1 d 视神经轴突内空泡变性,轴膜与髓鞘之间形成间隙,髓鞘松解;伤后3 d 轴突肿胀,空泡样变增多,髓鞘松解明显;伤后1周轴突髓鞘半环行套叠,泡状解离,有大量崩解产物出现,轴突呈空泡样和均质状,微丝、微管消失;伤后2周髓鞘呈现“洋葱皮”样改变;4周后髓鞘向心性扩展挤压,轴浆消失,整体崩解。结论家猫外伤性视神经病模型与临床视神经损伤具有相近的生物学特性,可以进行后续治疗等相关研究。伤后1 d 以上的视神经病理生理改变基本一致,只是量和度有所不同,故视神经损伤后应及早进行手术减压,以免延误最佳治疗时间。
Objective To make an animal model of traumatic optic neuropathy (TON) and observe its electrophysiological and morphological changes to provide a reference for clinical treatment. Methods Two adult cats were selected for anatomy of the optic nerve. Thirty adult cats were selected. The maxillary sinus and nasal septum were used to double-approach the optic nerve. The optic nerve of the inner segment of the optic nerve was injured with a homemade optic canal injury monitor and the TON model was established . The pupillary changes were observed and the changes of pattern reversal visual evoked potential (PR-VEP) at 1 h, 1 d, 3 d, 1 week, 2 weeks and 4 weeks after injury were observed. Animals were sacrificed on day 1, day 3, week 1, week 2 and week 4 to observe morphological changes of optic nerve. Results After the injury, eight cats had Margus-Gunn hamartilai ankylosis, and the other 22 eyes were neither direct nor indirect light reflex. The amplitude of N_ (75) P_ (100) and P_ (100) N_ (145) of VEP wave decreased by more than 50%, N_ (75), P_ (100) and N_ (145) The latency prolonged for more than 10 ms, and the waveform after two weeks tended to be a straight line. Under light microscope, the optic nerve tissue showed vacuolar degeneration over time, and its scope gradually expanded. From 1 day after injury, the optic nerve fiber bundle gradually swell and the fibrous vacuoles degenerated. After 1 week, the vacuolization degenerated into flake; 2 weeks after the emergence of large vacuoles, and the formation of large vacuoles. Electron microscopy showed the degeneration of optic nerve axon within 1 d after injury, with a gap between axon and myelin sheath and release of myelin sheath. Axon swelling and vacuolization increased, and myelin sheath release was obvious on the 3rd day after injury. 1 week after injury, the axons of myelin sheaths were nested in a half-loop, bubble-shaped dissociation, a large number of disintegration products appeared, the axons were vacuole-like and homogeneous, microfilaments and microtubules disappeared; myelin sheath appeared 2 weeks after injury “Onion skin ” like change; 4 weeks after the radial expansion of myelin crush, axonal disappear, the overall disintegration. Conclusion The domestic cats with traumatic optic neuropathy model and clinical optic nerve injury have similar biological characteristics, which can be followed-up treatment and other related research. Pathological changes in the optic nerve more than 1 d after injury basically the same, but the amount and degree are different, so the optic nerve injury surgery should be as soon as possible decompression, so as not to delay the best treatment time.