Lee W R, Blass G E, Shaw D C
Department of Ophthalmology, University of Glasgow.
Eye (Lond). 1987;1 ( Pt 2):296-303. doi: 10.1038/eye.1987.48.
Second and third order retinal arterioles and venules were studied by immunohistochemistry and electron microscopy in the uncomplicated ageing process and in association with central retinal vascular occlusive disease (CRVOD). Tissue was obtained from eight enucleated human eyes (4 control, 4 with manifestations of CRVOD) and the investigation was directed towards abnormalities in the myocytes and the nature of collagenous materials which are deposited during the process of hyalinization. In normal ageing and in two cases of CRVOD, the endothelial cell monolayer and the underlying cells (subendothelial myocytes) were preserved in arterioles and venules: there was no evidence of fibrin leakage. Degenerative changes were found in the medial myocytes in control tissue from the fifth decade and these included myocyte shrinkage, accumulation of intracytoplasmic membranous structures, cytoplasmic vacuolation and fragmentation. The 'hyalinized' acellular vessel wall seen in CRVOD contains scattered activated fibroblast-like myocytes and macrophages lying within a matrix of fibronectin, 65 nm collagen and multilayered basement membrane material. Endothelial cells and cohort subendothelial myocytes are involved in the formation of capillaries which bud into the hyalinized vessel wall in CRVOD. In two cases of CRVOD there was extensive cellular degeneration and cell debris accumulated within the degenerate stroma: this was attributed to superadded total ischaemia. The pathogenesis of hyalinization remains obscure but a subtle age-related dysfunction of the morphologically intact lining endothelium could be responsible for metabolic damage to myocytes in the media.
采用免疫组织化学和电子显微镜技术，对单纯衰老过程以及与视网膜中央血管阻塞性疾病（CRVOD）相关的视网膜二级和三级小动脉及小静脉进行了研究。组织取自8只摘除的人眼（4只对照，4只患有CRVOD表现），研究针对肌细胞异常以及玻璃样变过程中沉积的胶原物质的性质。在正常衰老以及2例CRVOD病例中，小动脉和小静脉中的内皮细胞单层及下层细胞（内皮下肌细胞）得以保留：没有纤维蛋白渗漏的证据。在50岁起的对照组织中，发现中层肌细胞有退行性改变，包括肌细胞萎缩、胞质内膜性结构积聚、细胞质空泡化和碎片化。CRVOD中所见的“玻璃样变”无细胞血管壁包含散在的活化成纤维细胞样肌细胞和巨噬细胞，它们位于纤连蛋白、65nm胶原和多层基底膜物质的基质中。内皮细胞和相关的内皮下肌细胞参与了毛细血管的形成，这些毛细血管向CRVOD中的玻璃样变血管壁内出芽。在2例CRVOD病例中，存在广泛的细胞变性，退变的基质内积聚了细胞碎片：这归因于叠加的完全缺血。玻璃样变的发病机制仍不清楚，但形态完整的内衬内皮细胞轻微的年龄相关功能障碍可能是导致中层肌细胞代谢损伤的原因。
