@article{， author = {Smith, L E和Wesolowski, E和McLellan, A和Kostyk, S K和D'Amato, R和Sullivan, R和D'Amore, P A}，标题=“{小鼠氧诱导视网膜病变。}"，期刊= {Investigative Ophthalmology & Visual Science}， volume = {35}， number = {1}， pages = {101-111}， year = {1994}， month = {01}， abstract = "{PURPOSE:在具有可再生和可量化增殖性视网膜新生血管的小鼠中发展氧致视网膜病变，适合于研究早产儿视网膜病变(ROP)和其他血管病变的视网膜新生血管的发病机制和治疗干预。方法:将1周龄的C57BL/6J小鼠置于75 %氧环境中5天，然后置于室内空气中。一种新的荧光素-葡聚糖灌注方法已被开发来评估血管模式。在6微米的矢状横切面上，通过计数从视网膜延伸到玻璃体的新血管核来量化增殖性新生血管反应。横切面染色观察胶质纤维酸性蛋白(GFAP)。结果:荧光素-葡聚糖血管造影术描绘了整个血管模式，包括平板视网膜上的新生血管簇。高氧诱导的新生血管发生在血管化和无血管的视网膜交界处的中周缘。所有幼鼠均在出生后17 ~ 21天发生视网膜新生血管。在高氧状态下，9只眼每横截面平均有89个新生血管核，而在正常缺氧状态下，8只眼每横截面平均只有不到1个新生血管核(P \\< 0.0001)。 Proliferative vessels were not associated with GFAP-positive astrocyte processes. CONCLUSIONS: The authors have described a reproducible and quantifiable mouse model of oxygen-induced retinal neovascularization that should prove useful for the study of pathogenesis of retinal neovascularization as well as for the study of medical intervention for ROP and other retinal angiopathies. }", issn = {1552-5783}, eprint = {https://arvojournals.org/arvo/content\_public/journal/iovs/933177/101.pdf}, }