purpose. To test the hypothesis that early rod dysfunction predicts the blood vessel abnormalities that are the clinical hallmark of retinopathy of prematurity (ROP).

methods. Two rat models of ROP, induced by exposure to alternating 50%/10% oxygen (50/10 model) from postnatal day (P) 0 to P14, or exposure to 75% oxygen (75 model) from P7 to P14, and controls reared in room air were studied. In a longitudinal design, electroretinographic (ERG) records and digital fundus images were obtained at P20±1, P30±1, and P60±1. Rod sensitivity was derived from the ERG a-wave. Integrated curvature for the arterioles was calculated using Retinal Image multi-Scale Analysis (RISA) software.

results. In both ROP models, rod sensitivity was low at P20. Sensitivity improved by P60 in the 50/10 model, but remained low in the 75 model. Integrated curvature was high at P20 in both ROP models, decreased nearly to normal by P30 in the 50/10 model, but remained high in the 75 model, even at P60. At P20, rod sensitivity correlated with integrated vessel curvature. Furthermore, low rod sensitivity at P20 predicted abnormal retinal vasculature—that is, high integrated curvature—at P30 and P60. In contrast, vessel curvature at P20 did not predict sensitivity at P30 or P60.

conclusions. The rods may instigate the vascular abnormalities that are the clinical hallmark of ROP.