Experimental rubeosis of the iris in rabbits.

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.