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实验性视神经萎缩中视盘苍白的机制。一项荧光素血管造影研究。

The mechanism of disc pallor in experimental optic atrophy. A fluorescein angiographic study.

作者信息

Radius R L, Anderson D R

出版信息

Arch Ophthalmol. 1979 Mar;97(3):532-5. doi: 10.1001/archopht.1979.01020010276019.

DOI:10.1001/archopht.1979.01020010276019
PMID:105695
Abstract

Ascending optic atrophy was produced in 13 eyes of owl monkeys (Aotestrivirgatus) by retinal photocoagulation. Color fundus photography and fluorescein angiography were used to study and document the evolution of nerve head abnormalities. The optic nerve heads were also studied histopathologically. Except in certain instances of early transient (relative) filling defects, normal disc fluorescent patterns were preserved, despite clinically apparent optic nerve head pallor. Sectorial defects did not persist into the later phases of the angiogram. These findings may suggest a reduced blood flow, but neither angiographic nor histopathologic studies detected a reduced vascularity in the atrophic optic nerve. Pallor of the optic nerve head seems to result from alterations in the tissue reflectance and translucency following axonal loss and glial reorganization rather than from a decreased microvascular bed.

摘要

通过视网膜光凝术在夜猴(Aotus trivirgatus)的13只眼中造成了上行性视神经萎缩。使用彩色眼底照相术和荧光素血管造影术来研究并记录视乳头异常的演变过程。对视神经乳头也进行了组织病理学研究。除了某些早期短暂性(相对性)充盈缺损的情况外,尽管临床上视乳头明显苍白,但仍保留了正常的视盘荧光模式。扇形缺损在血管造影后期并未持续存在。这些发现可能提示血流减少,但血管造影和组织病理学研究均未检测到萎缩性视神经血管减少。视乳头苍白似乎是轴突丧失和胶质细胞重组后组织反射率和透明度改变所致,而非微血管床减少所致。

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Graefes Arch Clin Exp Ophthalmol. 2016 Aug;254(8):1609-1616. doi: 10.1007/s00417-016-3366-2. Epub 2016 Apr 26.
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视神经苍白(视神经萎缩)患者的视觉功能。
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