RETINAL OXYGEN DISTRIBUTION

Abstract

To study the role of oxygen distribution in the physiopathology of retinal vasoproliferative microangiopathies. Experimental retinal branch vein occlusion was induced in miniature pigs, using argon laser photocoagulation. The microvascular modifications, the retinal histologic features, and the retinal oxygen distribution were studied within 48 hours of the occlusion, and 3 weeks later. The retinal oxygen distribution modifications were also studied in ischemic retinal areas treated by scatter argon laser photocoagulation. Impaired regulation and blood flow decrease in the vascular bed that was affected by a retinal branch vein occlusion and tissue hypoxia led to modifications of oxygen delivery resulted in a damage of the neuronal cells, whereas the abnormal permeability of the affected retinal vessel wall induced extracellular edema and disorganization of the inner retina. Three weeks after vein occlusion, retinal neovascularization occurred in ischemic/hypoxic retinas. The "critical PO2" (tissue oxygen partial pressure), which induces neovascularization in miniature pigs has not been determined. Photocoagulation of the ischemic retinal territories induced an increase of preretinal oxygen partial pressure, which is restored to the normal preretinal values. A retinal branch vein occlusion in miniature pigs represents a reproducible experimental model of retinal neovascularization. Oxygen partial pressure measurements of the ischemic retina confirmed the hypothesis that tissue hypoxia triggers neovascularization; laser photocoagulation should be applied over the whole ischemic retinal areas to eliminate hypoxia in the inner retina.