Evaluation of the retina and optic nerve in a rat model of chronic glaucoma using in vivo manganese-enhanced magnetic resonance imaging

被引:85
作者
Chan, Kevin C.
Fu, Qing-ling
Hui, Edward S.
So, Kwok-fai [2 ]
Wu, Ed X. [1 ]
机构
[1] Univ Hong Kong, Dept Elect & Elect Engn, Lab Biomed Imaging & Signal Proc, Hong Kong, Hong Kong, Peoples R China
[2] Univ Hong Kong, Dept Anat, Hong Kong, Hong Kong, Peoples R China
关键词
chronic glaucoma; rat; intraocular pressure; optic nerve; fast axonal transport; manganese-enhanced magnetic resonance imaging;
D O I
10.1016/j.neuroimage.2008.01.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Glaucoma is a neurodegenerative disease of the visual system. While elevated intraocular pressure is considered to be a major risk factor, the primary cause and pathogenesis of the disease are still unclear. This study aims to employ in vivo manganese-enhanced magnetic resonance imaging (MEMRI) to evaluate dynamically the Mn2+ enhancements in the visual components following an induction of ocular hypertension in a rat model of chronic glaucoma. The episcleral and limbal veins were photocoagulated unilaterally in the right eye using an argon laser to maintain a consistent elevation of intraocular pressure by about 1.6 times above the normal level. Two and six weeks after glaucoma induction, MnCl2 solution (50 mM, 3 mu L) was injected intravitreally into both eyes, and MEMRI was performed 2 to 5 h after injection. Results showed a delayed increase in T1-weighted signal intensity in the glaucomatous optic nerve at 6 weeks but not 2 weeks after glaucoma induction. In addition, there was an accumulation of Mn2+ ions in the vitreous humour of the glaucomatous eye, with a high concentration of Mn2+ ions at the optic nerve head and the retina. These MEMRI findings may help understand the disease mechanisms, monitor the effect of drug interventions in glaucoma models and complement the conventional techniques in examining the glaucomatous visual components. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:1166 / 1174
页数:9
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