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目前,关于原发性开角型青光眼发病机理的理论多数以房水排出通道上的一些病理变化为基础,例如小梁胶原纤维增多、小梁片层玻璃样变性、围绕小梁轴心的基质增加,邻管组织中小梁内皮细胞层之间的均质嗜锇斑块沉积、Schlemm管萎陷等,而这些变化又多与小梁内皮细胞的形态、功能变化有关,使人们感到深入研究小梁内皮细胞十分重要。但仅从体内标本常难以分辨小梁内皮细胞的病变是原发性变化还是高眼压引起的继发性变化,不能
At present, most of the theories about the pathogenesis of primary open-angle glaucoma are based on some pathological changes in aqueous humor discharge channels such as increased trabecular collagen fibers, trabecular-degeneration-like hyalinization, matrix around the trabecular axis Increase, the adjacent tube trabecular endothelial cell layer homogenized alginate plaque deposition, Schlemm tube collapse, etc., and these changes and more with the trabecular endothelial cell morphology, functional changes, make people feel more in-depth study of small Beam endothelial cells are important. However, it is often difficult to tell whether the lesion of trabecular endothelial cells is the primary change or the secondary change caused by ocular hypertension only from in vivo specimens.