J. Browning et al., QUANTIFICATION OF OXYGEN-INDUCED RETINOPATHY IN THE MOUSE, Investigative ophthalmology & visual science, 38(6), 1997, pp. 1168-1174
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.