Division of Brain Development and Neuroregeneration, Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Tokyo, Japan.
Br J Ophthalmol. 2012 Apr;96(4):597-603. doi: 10.1136/bjophthalmol-2011-300831. Epub 2012 Jan 4.
To elucidate the morphological features of optic neuropathy in an ischaemic model of glaucoma in macaque monkeys.
The regional degenerative process was investigated by experimentally occluding the paraoptic branches of the lateral short posterior ciliary artery, that is, the circle of Haller and Zinn, in 11 eyes. Morphological changes in nerve fibres in the lamina cribrosa were evaluated by histopathology, immunocytochemistry and angiography, and the findings were compared with those observed in an aged macaque with spontaneous glaucomatous optic neuropathy.
Retinal ganglion cell axons were grouped in bundles and traversed through pores in columns of the lamina cribrosa. The processes of astrocytes extended to the bundles, and capillaries branched in surrounding connective tissue from the circular arterioles. Experimental ischaemia induced time-dependent anoxic deterioration of phosphorylated fibres in the temporal arcuate zone, accompanied by glial proliferation. A monkey with spontaneous visual impairment had nerve fibre loss and gliosis with collagenous proliferation in the temporal hemisphere, suggesting glaucomatous neuropathy.
Circulatory interference in the circle of Haller and Zinn caused time-dependent deterioration in the area where anoxic segmental degeneration is associated with pathogenesis of open-angle glaucoma.
阐明猴缺血性青光眼模型中视神经病变的形态学特征。
通过实验性阻断外侧短后睫状动脉的副视支，即 Haller 和 Zinn 环，在 11 只眼中研究区域性退行性过程。通过组织病理学、免疫细胞化学和血管造影评估视盘筛板中神经纤维的形态变化，并将观察结果与自发性青光眼性视神经病变的老年猴进行比较。
视网膜神经节细胞轴突成束穿过筛板的孔，星形胶质细胞的突起延伸到束中，毛细血管从环动脉分支到周围的结缔组织。实验性缺血导致颞弓形区磷酸化纤维的时间依赖性缺氧恶化，伴有胶质增生。一只患有自发性视力障碍的猴子在颞叶半球出现神经纤维丢失和神经胶质增生伴胶原性增殖，提示青光眼性神经病。
Haller 和 Zinn 环的循环干扰导致与开角型青光眼发病机制相关的缺氧节段性变性区域的时间依赖性恶化。
