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Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat
S Zhang1, D A Leske, W L Lanier
1Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Insights
Postnatal growth retardation significantly increases the incidence of retinopathy caused by metabolic acidosis in neonatal rats. This finding highlights growth retardation as a critical risk factor for preretinal neovascularization in immature eyes.
Area of Science:
- Neonatal physiology
- Ophthalmology
- Developmental biology
Background:
- Metabolic acidosis can induce retinopathy in neonatal rats, mirroring retinopathy of prematurity (ROP).
- Previous research indicated that postnatal growth retardation exacerbates oxygen-induced retinopathy.
Purpose of the Study:
- To investigate the impact of postnatal growth retardation on the incidence and severity of acidosis-induced retinopathy.
- To determine if growth retardation is a risk factor for preretinal neovascularization in the context of metabolic acidosis.
Main Methods:
- 100 Sprague-Dawley rats were divided into standard and expanded litters to induce growth retardation.
- Rats received NH(4)Cl to induce metabolic acidosis from days 2-7.
- Retinal vasculature, neovascularization (NV), and vascularized areas were assessed post-recovery using ADPase staining and microscopy.
Main Results:
- Neovascularization (NV) occurred in 52% of rats in expanded litters versus 18% in standard litters (p=0.005).
- Pups in expanded litters showed significantly lower body weight, confirming growth retardation (e.g., 10.8g vs 13.4g on day 8, p<0.001).
Conclusions:
- Postnatal growth retardation elevates the incidence of acidosis-induced retinopathy in neonatal rats.
- This study reinforces postnatal growth retardation as a risk factor for preretinal neovascularization, consistent with clinical observations in premature infants and ROP.
Purpose:
We have previously described a metabolic acidosis-induced retinopathy in the neonatal rat, similar to retinopathy of prematurity (ROP). We also have reported exacerbation of oxygen-induced retinopathy by postnatal growth retardation, produced by raising newborn rats in 'expanded' litters. In the present study, we investigated the effect of postnatal growth retardation on the incidence and severity of acidosis-induced retinopathy.
Methods:
100 newborn Sprague-Dawley rats were randomly assigned to two expanded litters of 25 pups each and five standard control litters of 10 pups each. All rats were gavaged with 10 mM/kg NH(4)Cl twice daily from days two to seven. Following five days of recovery, retinal vasculature was assessed using ADPase staining, light microscopy, and computer-assisted image analysis. The presence of neovascularization (NV), severity of NV (clock hours), and 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 pups in expanded litters was confirmed by comparing total body weight of pups raised in expanded and standard control litters (10.8g vs 13.4g on day 8, p < 0.001; 20.8g vs 25.2g on day 13, p = 0.002).
Conclusions:
Postnatal growth retardation increases the incidence of acidosis-induced retinopathy in the neonatal rat. Our study provides further evidence that postnatal growth retardation is a risk factor for preretinal neovascularization in immature retinae and is consistent with the clinical observation that the smallest and sickest premature infants are more likely to suffer from ROP.