A rat model of chronic pressure-induced optic nerve damage
A rat model of chronic pressure-induced optic nerve damage
复制标题
DOI：
10.1006/exer.1996.0184
复制
发表时间：
1997-01-01
影响因子：
3.4
通讯作者：
Johnson, EC
中科院分区：
文献类型：
--
作者：
Morrison, JC;Moore, CG;Johnson, EC
为了引起大鼠单侧长期升高的眼压，在锁膜外静脉注射高渗生理盐水，用Tone-Pen XL眼压计监测眼压。对不同程度和持续时间的眼内压升高进行组织学分析，以确定这些压力对视神经的影响。在连续的20只动物中，有9只动物在一次注射后眼压升高，而随后的注射使另外7只动物的眼压升高。一只眼睛变得低垂。在剩下的动物中，故意不进行足以升高眼压的后续注射，以确定注射对视神经可能的直接影响。平均持续血压升高范围为7至28毫米汞柱，所有眼睛的视网膜血管保持灌注。没有眼压升高的眼睛的视神经横切面与未注射的眼睛的视神经横切面相同，而眼压升高最大的眼睛的神经显示轴突损伤，涉及100%的神经区域。眼压升高不严重或持续时间较短的眼睛显示部分损伤，神经区域的范围为0.5%至10.4%。70%的神经损伤集中在颞上区。在视神经头部，通常与星形胶质细胞相关，轴突含有异常的膜结合囊泡和线粒体。前房角显示小梁网硬化，伴有前粘连，但施勒姆管、收集器通道和水静脉通畅。视神经损伤大鼠的单侧小梁网硬化产生持续的眼压升高，在许多方面与人类青光眼相似。了解该模型的神经损伤机制可能为人类青光眼的发病机制提供新的认识。(C) 1997学术出版社有限公司
To develop unilateral, chronically elevated intraocular pressure in rats, episcleral veins were injected with hypertonic saline and the intraocular pressure was monitored with a Tone-Pen XL tonometer. Histologic analyses of eyes with differing degrees and durations of intraocular pressure elevation were performed to ascertain the effects of these pressures on the optic nerve. Out of 20 consecutive animals, nine had elevations of intraocular pressure following a single injection, while subsequent injections raised intraocular pressure in seven others. One eye became hypotonous. In the remaining animals, subsequent injections sufficient to raise intraocular pressure were deliberately withheld, to determine the possible direct effects of injections on the optic nerve. Mean sustained pressure elevations ranged from 7 to 28 mm Hg and the retinal vasculature remained perfused in all eyes. Optic nerve cross sections from eyes without intraocular pressure elevation appeared identical to those from uninjected eyes, while nerves from eyes with the greatest intraocular pressure rise demonstrated axonal damage that involved 100% of the neural area. Eyes with either less severe pressure elevations or shorter durations showed partial damage, ranging from 0.5% to 10.4% of the neural area. In 70% of these nerves, damage was concentrated in the superior temporal region. Within the optic nerve head, often associated with astrocytes, axons contained abnormal accumulations of membrane-bound vesicles and mitochondria. The anterior chamber angles showed sclerosis of the trabecular meshwork with anterior synechiae, but Schlemm's canal, collector channels and aqueous veins appeared patent. Unilateral sclerosis of the trabecular meshwork produces sustained elevation of intraocular pressure in rats with optic nerve damage that in many ways resembles that seen in human glaucoma. Understanding the mechanism of nerve damage in this model may provide new insights into the pathogenesis of human glaucoma. (C) 1997 Academic Press Limited