Hyperoxia‐induced Retinal Microvasculopathy Correlates with Lung Injury and Inflammation in Neonatal Mice

Abstract

ObjectivePremature infants with respiratory failure require oxygen supplementation, which can destroy developing lungs and lead to acute lung injury (ALI). Continued oxygen use also damages retinal tissue by disrupting normal angiogenesis, leading to retinopathy of prematurity (ROP). Using a mouse model of oxygen‐induced retinopathy (OIR) and ALI, we assessed the correlation between retinal microvascular abnormalities in vivo and lung tissue injury ex vivo.MethodsNeonatal C57BL6/J mice were exposed to 75% oxygen from postnatal day 7 (P7) to P12 and then exposed to room air until P17. Fluorescein angiography (FA) images of the retinal vasculature were acquired in vivo. Bronchoalveolar lavage (BAL) was performed on the mice lung tissue ex vivo, followed by cytometry and protein estimation of the BAL fluid. The total cell count was used as a measure of lung inflammation; while total protein estimation was used to assess lung injury.ResultsIn vivo FA imaging of retinal vasculature revealed aberrant neovascularization and regions of capillary network loss in mice exposed to hyperoxia compared to room air exposed controls (Figure 1A). There was a 4‐fold increase in total inflammatory cells (Figure 1B) and a 3‐fold increase in protein levels in BAL fluids of hyperoxia‐exposed mice compared to room air controls.ConclusionsOur findings demonstrate a correlation between retinal microvasculopathy and lung tissue injury and inflammation in neonates, suggesting in vivo imaging of retinal microvasculature could be a potential biomarker for lung injury.Source of Research Support: R01 HL66109, R01 ES011863 and R01 EY017918