Fuchs U, Reichenbach A, Siwula H, Taubert G, Winiecki P
Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1981;216(3):245-51. doi: 10.1007/BF00408166.
A quantitative exploration of retinal cell content was carried out in diabetics and metabolically healthy controls of the same age and sex distribution. After diabetes of 6 years duration there was a drastic diminution of cells in the ganglion cell layer of the central retinal area, while the number of cells of the inner nuclear layer was slightly reduced and that of the outer nuclear layer was still unchanged. The periphery of short duration diabetic retinae showed a normal cell content in all nuclear layers. In long-term diabetes (about 10 years), significant diminutions in cell numbers were found in all layers of both the retinal center and periphery. The described cell deficits are accounted for by disturbances of retinal microcirculation. After a relatively short duration of diabetes, blood flow interruptions in the area supplied by the central retinal artery occur; in long-term diabetics the chorioidal vessels are also affected. Connexions between the cell-deficit pattern and functional (electrophysiological) findings are discussed.
对年龄和性别分布相同的糖尿病患者及代谢健康的对照者进行了视网膜细胞含量的定量研究。糖尿病病程6年后，视网膜中央区域神经节细胞层的细胞数量急剧减少，而内核层细胞数量略有减少，外核层细胞数量仍未改变。病程较短的糖尿病视网膜周边区域所有核层的细胞含量均正常。在长期糖尿病（约10年）中，视网膜中央和周边所有层的细胞数量均显著减少。上述细胞缺陷是由视网膜微循环紊乱所致。糖尿病病程相对较短时，视网膜中央动脉供血区域会出现血流中断；长期糖尿病患者脉络膜血管也会受到影响。文中还讨论了细胞缺陷模式与功能（电生理）结果之间的联系。
