首都医科大学学报 ›› 2002, Vol. 23 ›› Issue (1): 45-48.

• 临床研究 • 上一篇    下一篇

电镜观察糖尿病模型大鼠神经网膜的超微结构

卢艳, 姬志娟, 吴航, 赵志炜, 盛树力   

  1. 首都医科大学宣武医院眼科
  • 收稿日期:2001-12-17 修回日期:1900-01-01 出版日期:2002-01-15 发布日期:2002-01-15

Pathologic Changes of Neuroretina of Wistar Rats in Prodromal Stage of DR

Lu Yan, Ji Zhijuan, Wu Hang, Zhao Zhiwei, Sheng Shuli   

  1. Department of Ophthalmology, Xuanwu Hospital, Capital University of Medical Sciences
  • Received:2001-12-17 Revised:1900-01-01 Online:2002-01-15 Published:2002-01-15

摘要: 为观察糖尿病大鼠早期视网膜神经细胞的损害是否早于视网膜微循环改变,用链脲佐菌素(STZ,60mg/kg)建立糖尿病动物模型,分别于模型建立后1周、2周、1月处死大鼠,电镜观察大鼠视网膜及其微血管的变化。结果:与正常对照组比较,糖尿病大鼠于模型建立后1周、2周,其神经网膜神经细胞和视网膜微血管无明显改变;模型建立后1月,其视网膜色素上皮层、神经网膜微血管基底膜和周细胞无明显改变,但其神经网膜从外丛状层至神经纤维层有明显变化,表现为线粒体数目减少,线粒体肿胀,嵴变短、消失和髓样变性。神经纤维层和内、外网状层细胞突起水肿,在神经纤维层尤其明显,在神经节细胞层可见暗细胞形成。由于神经纤维层细胞突起水肿明显,压迫其周围微血管,导致微血管管腔狭窄,甚至闭锁,但微血管内皮细胞及基底膜未见异常。结果提示:糖尿病早期大鼠在视网膜神经细胞损害已发生时,视网膜微血管内皮细胞和基底膜超微结构未见异常,神经网膜神经细胞的损害可能是糖尿病视网膜病变(DR)的早期表现。

关键词: 糖尿病视网膜病变, 神经网膜, 病理改变

Abstract: The objective of the study was to observe whether the pathologic changes of neuroretina were earlier than those of microvessels in Wistar rats in prodromal stage of diabetic retinapathy(DR). Male wistar rats,weighing about 200 g, were injected intraperitoneally with STZ at 60 mg/kg to create diabetes. The Wistar rats were decapitated at the time of one week, two weeks, one month after the model created and the retina was removed for electron microscopic observation of the retina and it's microvessel changes. In comparison with the normal controls, there are no obvious changes in the retina and the microvessel of the wistar rats during one week and two weeks with diabtes. In the Wistar rats after one month with diabetes,there were no changes in pigment epithelium layer, rod cell and cone cell layer, outer nuclear layer and microvessel basement membrane and perivascular cells, but there were obvious pathologic changes from outer plexiform layer to neurofibrous layer: swelling and deformity of mitochondria, shortening and disappearance of cristae, medullary degeneration of mitochondria were seen, and the number of mitochondria were reduced. There was obvious neuron cell tuber edema in neurofibrous layer, outer and inner plexiform layer, especially in neurofibrous layer. Dark cells were seen in ganglionic layer. As a result of the edema, some adjacent microvessels were oppressed to be stenosed or even atretic. In the early stage of DR, there is no retina microvessel damage when retinal neuron damage happens. The retinal neuron damage could be the early sign in the progress of DR.

Key words: diabetic retinopathy, neurortetina, pathologic change

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