Abstract
Abstract: :
Purpose: To test the hypothesis that retinal hypoxia is a necessary and sufficient condition for the development of neovascularization (NV) in the newborn rat model of retinopathy of prematurity (ROP). Methods: Preretinal vitreous PO2 measurements were made during room air breathing using 19F magnetic resonance spectroscopy and a perfluoro-15-crown-5-ether droplet (0.3 µl) in normal adult and newborn (P1 - P20) rats, and in newborn rats exposured to 14 days of variable oxygen (before NV) or 6 additional days in room air after variable oxygen exposure (during NV). After each experiment, blood gas values were measured, retinas were isolated, ADPase stained, and flat mounted to determine peripheral avascular extent, and NV incidence and severity. Results: No significant differences were found in the average panvascular preretinal droplet derived PO2 between any of the groups in this study. These average oxygen tensions were similar to previously reported oxygen electrode values in the normal adult and P20 rat (IOVS 41:3999 (00)). However, evidence was found for retinal hypoxia at the peripheral extent of the retinal vessels from the optic nerve head during retinal vasculogenesis (P1-P10) and before the appearance of NV. No evidence for retinal hypoxia was found in the absence of NV (P14 or P20) or during the appearance of NV. Conclusion: The preretinal vitreous droplet derived PO2 values are accurate and obtainable from eyes that are too small to place an oxygen electrode. Since evidence for hypoxia at the vascular / avascular border was found both during vasculogenesis and before NV, hypoxia appears to be a necessary but not sufficient condition for the development of NV.
Keywords: 483 neovascularization • 428 hypoxia • 316 animal model