前部缺血性视神经病变的动物模型制作

发布时间：2018-06-30 09:21

本文选题：前部缺血性视神经病变 + 动物模型　；参考：《陕西中医学院》2006年硕士论文

【摘要】：目的：前部缺血性视神经病变(Anterior ischemic optic neuropathy，AION)简称缺盘，是临床常见的眼底病，目前对AION的治疗方法虽甚多，但效果并不理想。缺盘是由于视神经前部的视网膜神经节轴索细胞(retinal ganglion cell，RGC)的突然缺血引起的，这也是视神经功能紊乱的主要原因。过去一直没有简便、易得的视神经功能紊乱的动物模型，我们造成AION的动物模型，对这种病的发病机理，，发病因素进行更详细的研究，依其结果进行中西医结合的临床治疗研究，对探寻一种简便、有效的治疗缺盘的方法有着积极意义。方法：我们用较新颖的光动力方法制作出一种缺盘的鼠模型(rat model of AION，rAION)。将30只实验性SD大鼠随机分为4组，分别为空白对照组5例、激光组5例、光敏剂组5例、光动力模型组15例。动物均取右眼为实验眼，左眼为自身对照眼。光动力模型组从鼠尾静脉注入血卟啉衍生物(hematoporphyrin derivative，HPD)后，立即用氪红光647nm、80mw、投照占2／3视盘为准的光斑，持续照射鼠视盘120秒；激光组单纯用氪红光647nm、80mw、投照占2／3视盘为准的光斑，持续照射鼠视盘120秒；光敏剂组单纯从鼠尾静脉注入HPD；空白对照组未做任何处理。通过与对照组的比较，我们能够确定是光化学作用，而不是热损伤或光敏剂对细胞的毒性作用导致的视神经缺血，这种模型相似于人类的缺盘。用这种方法制作rAION模型，没有明显地损伤视网膜，也没有破坏视网膜下面的结构，使我们能很好的了解活体上RGC及视神经的反应。通过眼底荧光血管造影、组织学、视电生理等方法，我们可以描述同单个RGC轴索缺血相联系的早期改变的特征。结果：眼底：光动力模型组，造模后第1天，视盘上半水肿，边界不清；造模后第6天，视盘仍水肿；造模后第90天，视盘上半萎缩，色灰白。FFA：光动力模型组造模后半小时，即可见到鼠视盘上部高荧光，该鼠23d后视盘始终低荧光；造模后第1天视盘上部早期“低荧光”、中晚期“高荧光”；造模后第6天视盘上部“低荧光”。视电生理上的改变：在光动力模型组中，实验眼与自身对照眼相比，F-VEP P100的潜伏期延长(n=10，t=3.148，p=0.012)、波幅值降低(n=10，t=4.082，p=0.003)。这种变化从造模后早期一直持续到造模后35天。OCT：光动力模型组造模后第6天，鼠视盘视神经反射面高出视网膜反射面，且表面粗糙不平厚度增加。组织病理学改变：HE
[Abstract]:Objective: anterior ischemic optic neuropathy (Anterior ischemic optic neuropathysis) is a common clinical fundus disease. Although there are many methods to treat it, the effect is not satisfactory. The lack of disc is caused by the sudden ischemia of the retinal ganglion axonal cells (retinal ganglion) in the anterior part of the optic nerve, which is the main cause of the optic nerve dysfunction. In the past, there was no simple, easy to get animal model of optic nerve dysfunction. We made AION's animal model, and we studied the pathogenesis of the disease and the factors involved in it in more detail. According to the results, it is of positive significance to explore a simple and effective method for the treatment of missing disk. Methods: a new photodynamic method was used to produce a diskless mouse model (rat model of AION ion. Thirty experimental SD rats were randomly divided into 4 groups: blank control group (n = 5), laser group (n = 5), Guang Min group (n = 5) and photodynamic model group (n = 15). The right eye was used as experimental eye and the left eye as self-control eye. In the photodynamic model group, the hematoporphyrin derivative was injected into the tail vein of the rat, and then it was treated with krypton red light (647 nm) for 80 mw. the spot, which accounted for 2 / 3 of the optic disk, was irradiated continuously for 120 seconds. The laser group was treated with krypton red 647nmm-1 for 80mw, and the laser group was exposed to the light spot of 2 / 3 optical disk for 120 seconds, the Guang Min group was injected into the tail vein of the mouse for 120 seconds, and the blank control group did not do any treatment. Compared with the control group, we can confirm that the optic nerve ischemia caused by the photochemical action, not the thermal injury or the cytotoxicity of Guang Min, is similar to that of human dissection. Using this method to make rAION model, there is no obvious damage to the retina and the structure under the retina, so we can understand the reaction of RGC and optic nerve in vivo. By means of fundus fluorescein angiography histology and electrophysiology we can describe the characteristics of early changes associated with single RGC axonal ischemia. Results: the ocular fundus: in the photodynamic model group, on the first day after modeling, the upper optic disc was edema with unclear boundary, on the sixth day, the optic disc was still oedema; on the 90th day after modeling, the optic disc was half atrophied, and the color was gray. FFA: the photodynamic model group had half an hour after making the model. The high fluorescence of the upper part of the optic disk of the mouse can be seen, which is always low fluorescence after 23 days, "low fluorescence" of the upper part of the optic disk in the first day after modeling, "high fluorescence" in the middle and late period, and "low fluorescence" in the upper part of the disc on the 6th day after modeling. In the photodynamic model group, the latency of F-VEP P100 was longer than that of the control group (nm10t ~ (3.148) and the amplitude was decreased (n ~ (10) ~ (10) t ~ (4.082) P ~ (0.003). This change lasted from the early stage after modeling to 35 days after modeling. The optic nerve reflex surface of the optic disc in the photodynamic model group was higher than that of the retina reflex surface on the 6th day after the model making and the rough thickness of the surface was increased. Histopathological changes: he
【学位授予单位】：陕西中医学院
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R-332

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