QUANTIFICATION OF OXYGEN-INDUCED RETINOPATHY IN THE MOUSE

Purpose. To describe a quantifiable model of vascular proliferation in oxygen-induced retinopathy (OIR) in the mouse. Methods. Neonate Quack enbush mice were subjected to high-ambient oxygen (similar to 95%) for the first 5 days after birth, effecting a total inhibition of retinal vascular growth with. Animals then were returned to room air, and the rates of subsequent vascular development in the plane of the retina a nd estimates of retinal capillary density were measured from flatmount s of ink-perfused eyes. Observations were confirmed with fluorescein i sothiocyanate-lectin labeling of the peripheral vasculature. Abnormal growth of vascular sprouts into the vitreous was recorded from cross-s ections. Observations in OIR were compared against those of age-matche d control animals. Results. The slower rate of retinal revascularizati on in OIR mice was quantified and compared against the normal rate. Le ctin-binding studies confirmed the reliability of ink preparations. Th e number of vitreous sprouts in OIR peaked 8 to 10 days after animals were returned to room air (13 to 15 postnatal days). Sprouts then regr essed, to disappear by postnatal day 20, In all respects, bar a slight ly lower peripheral capillary density, the normal retinal vascular pat tern was achieved in OIR within 15 days of exposure to room air (as op posed to the 10 days required in control mice). Conclusions. The proto col described for quantifying retinal proliferation in mouse OIR is re produced readily, and the data recorded here will allow the effectiven ess of subsequent treatments that may affect retinal vascular growth t o be evaluated better.