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实验性急性眼压升高时视神经损伤的机制

The mechanism of optic nerve damage in experimental acute intraocular pressure elevation.

作者信息

Quigley H A, Flower R W, Addicks E M, McLeod D S

出版信息

Invest Ophthalmol Vis Sci. 1980 May;19(5):505-17.

PMID:6154668
Abstract

We produced intraocular pressure (IOP) elevations in 32 primate eyes and studied retinal ganglion cell rapid axonal transport with autoradiography and electron microscopy. Animals breathing room air at sea level pressure were compared to animals breathing 100% oxygen at 3 atm pressure in a hyperbaric chamber. Despite major increases in arterial oxygen levels in the hyperbarically oxygenated animals, both groups had axonal transport blockade at the optic nerve head. Anoxia appears not to be the most important cause of acute axonal damage induced by elevated IOP. The pattern of axonal abnormality within individual fiber bundles at the optic nerve head provides support for mechanical compression as a more likely alternative cause for induced neural damage.

摘要

我们使32只灵长类动物的眼睛眼压升高,并通过放射自显影和电子显微镜研究视网膜神经节细胞的快速轴突运输。将在海平面压力下呼吸室内空气的动物与在高压舱中呼吸3个大气压的100%氧气的动物进行比较。尽管高压氧合动物的动脉氧水平大幅升高,但两组在视神经乳头处均出现轴突运输阻滞。缺氧似乎不是眼压升高引起急性轴突损伤的最重要原因。视神经乳头处单个纤维束内轴突异常的模式支持机械压迫是诱发神经损伤更可能的另一个原因。

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