论文部分内容阅读
目的建立猫慢性视神经压迫损伤动物模型。方法成年健康猫20只,按置入球囊内注入不同剂量造影剂分为健康对照组、0.2ml、0.25ml、0.35ml 4个组,每组5只。模仿临床上翼点入路,显微手术暴露视神经后,置入充盈的不可脱球囊于其下,后接导管,以注入造影剂的方式控制球囊大小,形成类似鞍区肿瘤占位,并辅以CT和视觉诱发电位检查,研究慢性视神经损伤前后视觉电生理方面的变化。以上动物按分组处死后,取视神经标本,进行电镜分析,研究视神经损伤后的病理改变。结果早期(术后2周),因占位病变(0.2cm3)在颅内代偿范围内,视觉诱发电位改变不明显。术后4周颅内占位达0.3cm3时超出颅内代偿空间,视觉诱发电位改变,颅内占位达0.35cm3时视觉诱发电位改变更为明显,表现为P1波潜伏期明显延长,振幅明显减小。结论首次建立的慢性颅内段视神经压迫损伤模型稳定,可模仿鞍区肿瘤引起的视神经病变,慢性视神经压迫的视觉诱发电位改变呈渐进性,早期在代偿范围内改变并不明显,晚期表现为P1波潜伏期延长,振幅减小,如不去除压迫难以恢复。
Objective To establish an animal model of chronic optic nerve compression injury in cats. Methods Twenty adult healthy cats were divided into four groups according to different doses of contrast medium: 0.2ml, 0.25ml and 0.35ml. Five rats in each group. Imitate the clinical pterional approach, microsurgery expose the optic nerve, into the filling of the capsule can not be off under it, followed by the catheter to inject contrast medium to control the size of the balloon to form a similar saddle tumor space, And supplemented by CT and visual evoked potential test to study the changes of visual electrophysiology before and after chronic optic nerve injury. After the above animals were sacrificed in groups, optic nerve specimens were taken for electron microscopic analysis to study the pathological changes after optic nerve injury. Results Early (2 weeks after operation), visual evoked potential did not change significantly due to mass lesion (0.2cm3) within the range of intracranial compensation. 4 weeks after intracranial space occupying 0.3cm3 beyond the compensatory space of the brain, visual evoked potential changes, intracranial space occupying 0.35cm3 visual evoked potential changes more pronounced, the performance of P1 wave latency was significantly longer, amplitude significantly Decrease Conclusions The model of optic nerve compression injury in chronic intracranial optic nerve was established for the first time. It could mimic optic neuropathy induced by tumor in sellar region. The change of visual evoked potentials in chronic optic nerve compression was progressive. The changes in early compensatory range were not obvious. P1 wave latency, amplitude decreases, if not remove the pressure is difficult to recover.