300 LACK OF DRUG EFFECT ON OXYGEN INDUCED RETINAL ARTERY CONSTRICTION IN THE KITTEN

The initial injury in the animal model of oxygen induced retinopathy is thought to be irreversible arteriolar constriction. Since vitamin E is beneficial in this model, its effect on early arteriolar constriction, as well as the effect of prostaglandin inhibitors (as used in the beagle model) were tested. 3 day old kittens were placed in 80% oxygen and their retinas perfused with india ink 48hrs later. Pretreatment from day 1 with free tocopherol (vitamin E) 200 mg/kg/day IM, aspirin 20 mg/kg/day orally, or indomethacin 0.5 mg/kg/day orally was compared to no drug treatment in oxygen and room air controls. 5 kittens were randomly assigned to each group. Additionally, the effects of 8% carbon dioxide in combination with 21% oxygen (room air), 80% oxygen, or aspirin plus 80% oxygen was studied. All treatments except room air control and 8% carbon dioxide in room air O2 resulted in near total obliteration of patent retinal vessels, as demonstrated with the india ink perfusions. Kittens in 8% carbon dioxide with only 21% oxygen had moderate attenuation of the smallest vessels and partial closure of the arterioles. This unexpected failure of carbon dioxide to cause vasodilitation is unexplained. Vitamin E does not exert its beneficial effect on oxygen induced retinopathy in the kitten by maintaining vessel patencey during hyperoxia.