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目的:探讨糖尿病大鼠视网膜病变（diabetic retinopathy.DR.简称糖网病）,早期视细胞（视感受器）的超微结构病变,为糖网病光感受器功能障碍提供形态学依据。方法:选择清洁级SD大鼠随机分成正常对照组（CON）、糖尿病1月（DM1）、3月（DM3）和6月（DM6）。按60mg/kg腹腔内注射链脉佐菌素（STZ）诱导大鼠糖尿病,每组12只,取大鼠视网膜透射电镜观察。处死前每月测血糖和眼底镜检查1次。结果:病程1个月:视杆、视锥细胞的外节膜盘模糊不清,膜盘间隙略有扩大,椭圆体内中心粒和纤毛仍清晰可见,线粒体规则的排列在周围。病程3个月,视细胞外节膜盘间隙明显扩大,纵横交错,排列紊乱,并发生局灶性断裂,椭圆体内有部分线粒体肿胀、脱嵴。毛细血管扩张,神经纤维中心微管也有水肿。病程6个月:视细胞外节内膜盘断裂溃变,颜色淡,并出现许多泡沫状结构,椭圆体内的线粒体变小,排列不规则,有的脱嵴、水肿,毛细血管已有部分由扩张转为狭窄。结论:糖尿病早期毛细血管由局部扩张转为狭窄,视网膜因缺血、缺氧的加重导致视细胞超微结构的病理改变,并随病程的进展而加重。
OBJECTIVE: To investigate the ultrastructural changes of diabetic retinopathy (DR) and early optic cell receptor (PD) in diabetic rats and provide the morphological evidence for the dysfunction of photoreceptor in diabetic retinopathy. Methods: Clean SD rats were randomly divided into normal control group (CON), diabetes mellitus (DM1), March (DM3) and June (DM6). Diabetic rats were induced by 60 mg / kg intraperitoneal injection of streptozotocin (STZ), with 12 rats in each group. Retinal transmission electron microscopy was used to observe the diabetic rats. Blood glucose and ophthalmoscopy were performed once a month before sacrifice. Results: The course of disease was 1 month. The outer membrane segments of rods and cones were obscure, and the gap between membrane disks was slightly enlarged. The centrioles and cilia in the oval body were still clearly visible, and the mitochondria regularly arranged around them. Duration of 3 months, depending on the extracellular articular disk space was significantly expanded, criss-cross, arranged disorder, and the occurrence of focal rupture, some mitochondria in the oval body swelling, debridement. Telangiectasia, central nervous system microtubules also have edema. Duration of 6 months: depending on the extracellular endomembrane disc rupture, light color, and the emergence of many foam-like structure, the mitochondria in the ellipsoid smaller, irregular arrangement, and some debridement, edema, capillaries have been part of the Expansion into narrow. Conclusion: The early stage of diabetes mellitus changes from local dilatation to stenosis. Retinal ischemia and hypoxia lead to the pathological changes of the ultrastructure of optic nerve cells, which aggravate with the progress of the disease.