本文選題：前部缺血性視神經(jīng)病變 + 動(dòng)物模型�。� 參考：《陜西中醫(yī)學(xué)院》2006年碩士論文

【摘要】：目的：前部缺血性視神經(jīng)病變(Anterior ischemic optic neuropathy，AION)簡(jiǎn)稱(chēng)缺盤(pán)，是臨床常見(jiàn)的眼底病，目前對(duì)AION的治療方法雖甚多，但效果并不理想。缺盤(pán)是由于視神經(jīng)前部的視網(wǎng)膜神經(jīng)節(jié)軸索細(xì)胞(retinal ganglion cell，RGC)的突然缺血引起的，這也是視神經(jīng)功能紊亂的主要原因。過(guò)去一直沒(méi)有簡(jiǎn)便、易得的視神經(jīng)功能紊亂的動(dòng)物模型，我們?cè)斐葾ION的動(dòng)物模型，對(duì)這種病的發(fā)病機(jī)理，，發(fā)病因素進(jìn)行更詳細(xì)的研究，依其結(jié)果進(jìn)行中西醫(yī)結(jié)合的臨床治療研究，對(duì)探尋一種簡(jiǎn)便、有效的治療缺盤(pán)的方法有著積極意義。 方法：我們用較新穎的光動(dòng)力方法制作出一種缺盤(pán)的鼠模型(rat model of AION，rAION)。將30只實(shí)驗(yàn)性SD大鼠隨機(jī)分為4組，分別為空白對(duì)照組5例、激光組5例、光敏劑組5例、光動(dòng)力模型組15例。動(dòng)物均取右眼為實(shí)驗(yàn)眼，左眼為自身對(duì)照眼。光動(dòng)力模型組從鼠尾靜脈注入血卟啉衍生物(hematoporphyrin derivative，HPD)后，立即用氪紅光647nm、80mw、投照占2／3視盤(pán)為準(zhǔn)的光斑，持續(xù)照射鼠視盤(pán)120秒；激光組單純用氪紅光647nm、80mw、投照占2／3視盤(pán)為準(zhǔn)的光斑，持續(xù)照射鼠視盤(pán)120秒；光敏劑組單純從鼠尾靜脈注入HPD；空白對(duì)照組未做任何處理。通過(guò)與對(duì)照組的比較，我們能夠確定是光化學(xué)作用，而不是熱損傷或光敏劑對(duì)細(xì)胞的毒性作用導(dǎo)致的視神經(jīng)缺血，這種模型相似于人類(lèi)的缺盤(pán)。用這種方法制作rAION模型，沒(méi)有明顯地?fù)p傷視網(wǎng)膜，也沒(méi)有破壞視網(wǎng)膜下面的結(jié)構(gòu)，使我們能很好的了解活體上RGC及視神經(jīng)的反應(yīng)。通過(guò)眼底熒光血管造影、組織學(xué)、視電生理等方法，我們可以描述同單個(gè)RGC軸索缺血相聯(lián)系的早期改變的特征。 結(jié)果：眼底：光動(dòng)力模型組，造模后第1天，視盤(pán)上半水腫，邊界不清；造模后第6天，視盤(pán)仍水腫；造模后第90天，視盤(pán)上半萎縮，色灰白。FFA：光動(dòng)力模型組造模后半小時(shí)，即可見(jiàn)到鼠視盤(pán)上部高熒光，該鼠23d后視盤(pán)始終低熒光；造模后第1天視盤(pán)上部早期“低熒光”、中晚期“高熒光”；造模后第6天視盤(pán)上部“低熒光”。視電生理上的改變：在光動(dòng)力模型組中，實(shí)驗(yàn)眼與自身對(duì)照眼相比，F(xiàn)-VEP P100的潛伏期延長(zhǎng)(n=10，t=3.148，p=0.012)、波幅值降低(n=10，t=4.082，p=0.003)。這種變化從造模后早期一直持續(xù)到造模后35天。OCT：光動(dòng)力模型組造模后第6天，鼠視盤(pán)視神經(jīng)反射面高出視網(wǎng)膜反射面，且表面粗糙不平厚度增加。組織病理學(xué)改變：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
【學(xué)位授予單位】：陜西中醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類(lèi)號(hào)】：R-332

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