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巩膜静脉阻塞致眼压持续升高的小鼠模型

Mouse model of sustained elevation in intraocular pressure produced by episcleral vein occlusion.

作者信息

Ruiz-Ederra Javier, Verkman A S

机构信息

Department of Medicine and Physiology, Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0521, USA.

出版信息

Exp Eye Res. 2006 May;82(5):879-84. doi: 10.1016/j.exer.2005.10.019. Epub 2005 Nov 28.

DOI:10.1016/j.exer.2005.10.019
PMID:16310189
Abstract

We have developed an inducible mouse model of glaucoma based on episcleral vein cauterization (EVC). Intraocular pressure (IOP) elevation in adult mice was produced by cauterizing three episcleral veins. Serial IOP measurements were done by induction-impact tonometry. IOP was significantly elevated by 104+/-20% in 20 out of 23 mice (87%) within the first day after EVC, and remained elevated for 4 weeks, with mean IOP 94% higher in EVC-treated vs. contralateral control eyes. Aqueous outflow blockade was verified from the IOP response to pulsed fluid infusions into the anterior chamber. Retinal ganglion cell (RGC) loss, determined by retrograde labelling using Fluoro-Gold applied to the superior colliculous, was approximately 20% at 2 weeks after EVC. We conclude that episcleral vein occlusion in mice produces significant and sustained elevation in IOP associated with increased outflow resistance and RGC loss, and thus may be useful to model glaucoma in genetically modified and drug-treated mice.

摘要

我们基于巩膜外静脉烧灼术(EVC)开发了一种可诱导的青光眼小鼠模型。通过烧灼三条巩膜外静脉使成年小鼠眼压(IOP)升高。采用感应式眼压计进行连续眼压测量。在EVC术后第一天,23只小鼠中有20只(87%)眼压显著升高104±20%,并持续升高4周,EVC治疗组眼睛的平均眼压比对侧对照眼高94%。通过眼压对前房脉冲式液体输注的反应验证了房水流出受阻。使用荧光金逆行标记上丘来确定视网膜神经节细胞(RGC)损失,EVC术后2周约为20%。我们得出结论,小鼠巩膜外静脉阻塞会导致眼压显著且持续升高,伴有流出阻力增加和RGC损失,因此可能有助于在转基因和药物治疗的小鼠中模拟青光眼。

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