Neovaskularisation der Hornhaut

Abstract

The penetration of blood vessels in the cornea causes a reduction of transparency and as a result reduced vision or even blindness. Experiments were conducted on 120 New Zealand albino rabbits, separated into different groups. Doses of vasculogenic alkalis provoked burning of the corneas. The following methods were used: Split-lamp investigation of the cornea with fluorescein, fluorescein angiography of the corneal neovessels, light and electron microscopy. Left eyes served as a control. Right eyes were treated with heparin and methylprednisolone, cobalt dichloride, prooxygens and antioxidants. Application of heparin and methylprednisolone reversibly inhibited the process of neoangiogenesis but intensified the corneal ulcer. The application of cobalt dichloride stimulated angiogenesis in the cornea. Electron microscopic observations showed the generation of transport pathways through the walls of neovessels. The basement membrane of the neovessels was formed nearly 4 - 5 months after their growth. Fluorescein angiography showed first increased permeability from the walls of the neovessels and, 4 - 5 months later, poor penetration of the fluorescein through the vessels walls. The application of inhibitors of neoangiogenesis decreases the repair processes in corneal lesions with initial neovascularization. The angiogenic factors are distributed by diffusion in the corneal stroma and neovessels initiate from the nearest limbic vessels. With the support of fluorescein angiography we can specify the time of their formation. The process of regression of the neovessels should be investigated.