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.

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