Age-related retinal vasculopathy

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.