Abstract
Abstract: :
Purpose: To test the hypothesis that an abnormal retinal Δ;PO2 is a surrogate marker of retinal neovascularization (NV) in a newborn mouse model. Methods: In urethane anesthetized newborn C57BL/6J mice, fMRI was used to measure the change in oxygen tension (Δ;PO2) panretinally during a hyperoxic inhalation challenge. In normal P17 mice, 100% oxygen (n = 4) and carbogen (95% O2 : 5% CO2, n = 9) challenges were compared. In separate experiments, newborn mice exposed to 75% oxygen (P5-P12) and then room air (P12-P17) were studied at P17 using fMRI and a carbogen challenge (n = 6). After each fMRI experiment, arterial blood gas values were measured during a second carbogen challenge, the retinas were isolated, ADPase stained, and flat mounted to determine avascular area, and NV incidence and severity. Results: In normal newborn mice, carbogen breathing produced a 74% increase (P < 0.05) in panretinal Δ;PO2 over that found during pure oxygen breathing. In experimental mice, the NV incidence and severity was 100% (22/22) and 5 clockhours, respectively. No NV was found in control pups. The retinal Δ;PO2 during a carbogen challenge for control (77 ± 4 mm Hg, mean ± SEM) and experimental (141 ± 6 mm Hg, ) newborns were statistically different (P = 0.0003). No significant (P ≷ 0.05) differences in arterial blood gas values were found between the control and experimental groups. Conclusion: Control newborn mice exhibit normal vasoactivity to hyperoxic gas challenges. Experimental mice demonstrated a supernormal response to a carbogen challenge during the appearance of NV. These results support our hypothesis that an abnormal panretinal Δ;PO2 is a surrogate marker of retinal vascular complications.
Keywords: 483 neovascularization • 432 imaging methods (CT, FA, ICG, MRI, OCT, RTA, SLO, ultrasound) • 316 animal model