Kottow M H, DeLeon J
Albrecht Von Graefes Arch Klin Exp Ophthalmol. 1978 Dec 8;209(1):11-8. doi: 10.1007/BF00419158.
Rabbits were subjected to vascular injuries in an attempt to cause ocular ischemia and rubeosis. Occlusion of the ipsilateral common carotid artery showed fluorescein angiographic evidence of iris ischemia, but no rubeosis. Occlusion of two or more vortex veins caused iris ischemia, vasodilation, and angiographically visible neovascular capillaries on the iris. Histology confirmed the presence of thin-walled, superficial neovascular channels. The stimultaneous occlusion of the carotid artery and of two or more ipsilateral vortex veins also produced angiographic and histologic evidence of iris ischemia and neovascularization. These results confirm that venous flow impairment is a more efficient stimulus to neovascularization than ischemia due to arterial insufficiency. Nevertheless, in none of the animals could a neovascular response comparable to human rubeosis be elicited, and it is concluded that vascular lesions to the anterior segment are not an adequate model to study rubeosis.
为了引发眼部缺血和虹膜红变，对兔子进行了血管损伤实验。同侧颈总动脉闭塞显示荧光素血管造影有虹膜缺血的证据，但无虹膜红变。两条或更多涡静脉闭塞导致虹膜缺血、血管扩张以及虹膜上血管造影可见的新生血管毛细血管。组织学证实存在薄壁的浅表新生血管通道。同时闭塞颈动脉和两条或更多同侧涡静脉也产生了虹膜缺血和新生血管形成的血管造影及组织学证据。这些结果证实，静脉血流受损比动脉供血不足导致的缺血是更有效的新生血管形成刺激因素。然而，在任何动物中都无法引发与人类虹膜红变相当的新生血管反应，得出的结论是眼前段血管病变不是研究虹膜红变的合适模型。
