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

S. Zhang, D. A. Leske, W. L. Lanier, Jonathan M Holmes

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

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 NH4Cl 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 (10.8 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 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.

Original languageEnglish (US)
Pages (from-to)133-139
Number of pages7
JournalCurrent Eye Research
Volume22
Issue number2
DOIs
StatePublished - 2001

Fingerprint

Acidosis
Growth
Retinopathy of Prematurity
Apyrase
Computer-Assisted Image Processing
Incidence
Premature Infants
Sprague Dawley Rats
Retina
Microscopy
Body Weight
Staining and Labeling
Oxygen
Light

Keywords

  • Ammonium chloride
  • Metabolic acidosis
  • Neovascularization
  • Retinopathy of prematurity

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat. / Zhang, S.; Leske, D. A.; Lanier, W. L.; Holmes, Jonathan M.

In: Current Eye Research, Vol. 22, No. 2, 2001, p. 133-139.

Research output: Contribution to journalArticle

Zhang, S. ; Leske, D. A. ; Lanier, W. L. ; Holmes, Jonathan M. / Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat. In: Current Eye Research. 2001 ; Vol. 22, No. 2. pp. 133-139.
@article{c8891688df774de7a4bff3d8dfb2ffbb,
title = "Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat",
abstract = "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 NH4Cl 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 (10.8 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 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.",
keywords = "Ammonium chloride, Metabolic acidosis, Neovascularization, Retinopathy of prematurity",
author = "S. Zhang and Leske, {D. A.} and Lanier, {W. L.} and Holmes, {Jonathan M}",
year = "2001",
doi = "10.1076/ceyr.22.2.133.5531",
language = "English (US)",
volume = "22",
pages = "133--139",
journal = "Current Eye Research",
issn = "0271-3683",
publisher = "Informa Healthcare",
number = "2",

}

TY - JOUR

T1 - Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat

AU - Zhang, S.

AU - Leske, D. A.

AU - Lanier, W. L.

AU - Holmes, Jonathan M

PY - 2001

Y1 - 2001

N2 - 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 NH4Cl 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 (10.8 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 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.

AB - 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 NH4Cl 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 (10.8 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 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.

KW - Ammonium chloride

KW - Metabolic acidosis

KW - Neovascularization

KW - Retinopathy of prematurity

UR - http://www.scopus.com/inward/record.url?scp=0034820556&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034820556&partnerID=8YFLogxK

U2 - 10.1076/ceyr.22.2.133.5531

DO - 10.1076/ceyr.22.2.133.5531

M3 - Article

C2 - 11402390

AN - SCOPUS:0034820556

VL - 22

SP - 133

EP - 139

JO - Current Eye Research

JF - Current Eye Research

SN - 0271-3683

IS - 2

ER -