The functional consequences of vitreous hemorrhage on the retina were studied using a rabbit experimental model. The repartition of hemoglobinic iron inside the retina was assessed after the intravitreous injection of ⁵⁹Fe-labeled erythrocytes. Electroretinographic studies were performed both in vivo after the intravitreous injection of labeled blood and in vitro on albino rat isolated retina treated with Fe⁺⁺⁺ ions. Results indicate that hemoglobinic iron migrates from the vitreous to the retina and inside the retinal tissue from ganglion cells to deeper layers. It is also demonstrated that hemoglobinic iron has a significant functional toxicity on the retina.

We present a full analysis of the electrophysiological parameters recorded from light-exposed or non-exposed rats. This model is a useful tool to study in vivo retinal degeneration.

The effect of intravitreal injections of DMTU (dimethylthiourea) and SOD (superoxide dismutase), two free radical scavengers, was evaluated in a rat model of retinal ischemia induced by elevated intraocular pressure. The drugs were administered just before or just after a 60 min ischemia. At days 2 and 7 after reperfusion, retinal recovery was evaluated by electroretinography. At day 7, layer thicknesses and cell rows were measured from histologic sections of paraffin-embedded retinas. In the vehicle-treated control group, we observed a decrease in the inner retinal layers and b-wave amplitude impairment. SOD injection (6 units/eye) protected the retina from ischemia/reperfusion injury. At day 2 after reperfusion, electroretinographic recovery was more efficient when SOD was administered just after ischemia (99%) than after pretreatment with SOD (81%) (p<0.03). In the DMTU-treated group (75 microg/eye), only the pretreatment induced significant electrophysiologic (40%) (p<0.001) and morphologic recovery.

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