Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat

Purpose. We have previously described a metabolic acidosis-induced retinopa thy in the neonatal rat, similar to retinopathy of prematurity (ROP). We al so have reported exacerbation of oxygen-induced retinopathy by postnatal gr owth retardation, produced by raising newborn rats in "expanded" litters. I n the present study, we investigated the effect of postnatal growth retarda tion on the incidence and severity of acidosis-induced retinopathy. Methods. 100 newborn Sprague-Dawley rats were randomly assigned to two expa nded litters of 25 pups each and five standard control litters of 10 pups e ach. All rats were gavaged with 10 mM/kg NH4Cl twice daily from days two to seven. Following five days of recovery, retinal vasculature was assessed u sing ADPase staining, light microscopy, and computer-assisted image analysi s. The presence of neovascularization (NV), severity of NV (clock hours), a nd vascularized retinal areas, were evaluated in a masked manner. Results. NV occurred in 52% of rats in expanded litters versus 18% of rats in standard control litters (p = 0.005). Postnatal growth retardation of pu ps in expanded litters was confirmed by comparing total body weight of pups raised in expanded and standard control litters (10.8 g vs 13.4 g on day 8 , p < 0.001; 20.8 g vs 25.2 g on day 13, p = 0.002). Conclusions. Postnatal growth retardation increases the incidence of acidos is-induced retinopathy in the neonatal rat. Our study provides further evid ence that postnatal growth retardation is a risk factor for preretinal neov ascularization in immature retinae and is consistent with the clinical obse rvation that the smallest and sickest premature infants are more likely to suffer from ROP.