Hori S, Mukai N
Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1980;213(1):1-9. doi: 10.1007/BF02391205.
Seventeen Wistar inbred rats were made diabetic by a single injection of streptozotocin (50 mg/kg body weight) and were killed after periods of 3, 6, 9 or 12 months. Pathological changes in pericapillary Müller cells of the retina were studied using electron microscopy. Basement membrane-like material proliferated in the intercellular space of the Müller cell network and occasionally appeared to insinuate into the Müller cell cytoplasm far from capillary pericytes and endothelial cells. The part of the Müller cell that was enveloped by proliferating basement membrane-like material showed partial necrosis which was thought to contribute to the widening of the capillary wall. A breakdown of the retinal framework, which leads to capillary dilatation, was also thought to be associated with partial necrosis of Müller cells. Highly electron-dense bodies accumulated in the Müller cell cytoplasm which surrounded the retinal capillaries. Ultrastructurally, these dense bodies resembled lysosomes. Their increased number might reflect the altered metabolism of the diabetic retina.
通过单次注射链脲佐菌素（50毫克/千克体重）使17只Wistar近交系大鼠患糖尿病，并在3、6、9或12个月后处死。使用电子显微镜研究视网膜毛细血管周围Müller细胞的病理变化。基底膜样物质在Müller细胞网络的细胞间隙中增殖，偶尔似乎侵入远离毛细血管周细胞和内皮细胞的Müller细胞胞质。被增殖的基底膜样物质包绕的Müller细胞部分显示出部分坏死，这被认为导致了毛细血管壁的增宽。视网膜结构的破坏导致毛细血管扩张，也被认为与Müller细胞的部分坏死有关。高电子密度体聚集在围绕视网膜毛细血管的Müller细胞胞质中。在超微结构上，这些致密体类似于溶酶体。它们数量的增加可能反映了糖尿病视网膜代谢的改变。
