Objectives/Goals: Anemia occurs universally among preterm infants who are also at risk of severe retinopathy of prematurity (ROP), a vision-threatening morbidity. We aim to determine the effect of anemia and its treatment with iron on the anatomical and molecular development of retinopathy and subsequent retinal function. Methods/Study Population: Oxygen-induced retinopathy (OIR) was induced in rat pups per the well-validated 50/10 OIR model, through 14 days of cyclic hyperoxia (50% FiO2) and hypoxia (10% FiO2) followed by recovery in normoxia. Anemia was induced by phlebotomy from postnatal day (P) 3 to P20, to a target hematocrit of 18%. Half of the pups were housed with a dam receiving standard iron chow (40 mg/kg) and half with a dam receiving high iron chow (400 mg/kg). Rat pups were euthanized at P20 during the neovascular phase of OIR. Retinal vascular morphometry (percent avascular and neovascular areas) was compared between groups by two-way ANOVA. Future outcome measures include retinal single-cell sequencing, flow cytometry, and molecular measures. Results/Anticipated Results: Anticipated Results: We anticipate that iron deficiency anemia will reduce the severity of OIR and that high dose iron treatment will increase it. We anticipate that high-dose iron treatment will induce oxidative stress, induce inflammation, and reduce the hypoxia-like effect of iron deficiency and angiogenic markers. Discussion/Significance of Impact: Upon completion, the results of this study can inform clinicians regarding preclinical effects of isolated anemia and treatment with iron on the development of retinopathy. This research has the opportunity to improve visual outcomes in preterm infants by improving clinical care of this population in the neonatal intensive care unit.
Ingolfsland et al. (Wed,) studied this question.