Carbon dioxide-induced retinopathy in the neonatal rat

Jonathan M Holmes, Shuichen Zhang, David A. Leske, William L. Lanier

Research output: Contribution to journalArticle

75 Citations (Scopus)

Abstract

Purpose. Hypercarbia has been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of hypercarbia on the retinal vasculature of the neonatal rat to determine whether hypercarbia alone could induce preretinal neovascularization analogous to ROP. Methods. In a preliminary blood gas study, 8-11-day-old rats were exposed to specific levels of inspired O2 and either 0.2% CO2 or 10% CO2. Arterial blood gases were obtained, and a level of inspired O2 was determined that, when combined with inspired 10% CO2 would produce a PaO2 equivalent to room air (pure hypercarbia). In the formal retinopathy study, 300 newborn rats raised in 12 expanded litters (n = 25 each) were exposed for 7 days to either room air, 10% CO2 in 21% O2 and nitrogen (high-inspired CO2 group) or 10% CO2 in 12.5% O2 and nitrogen (pure-hypercarbia group). Each type of exposure was followed by recovery in room air for 5 days. Animals were sacrificed on day 13 and retinae were analyzed, using fluores cein perfusion and ADPase staining techniques. Results. Neovascularization occurred in 19% of rats in the high-inspired CO2 group, and 14% of rats in the pure-hypercarbia group, compared to 0% of rats exposed to room air alone (p = 0.001, Chi square). Conclusions. In the neonatal rat model, exposure to hypercarbia alone, followed by room air recovery, results in preretinal neovascularization similar to that seen in oxygen-induced retinopathy. Our results support the suggestion that hypercarbia may be a risk factor for retinopathy of prematurity.

Original languageEnglish (US)
Pages (from-to)608-616
Number of pages9
JournalCurrent Eye Research
Volume17
Issue number6
DOIs
StatePublished - 1998

Fingerprint

Hypercapnia
Carbon Dioxide
Retinopathy of Prematurity
Air
Recovery Room
Nitrogen
Gases
Apyrase
Retina
Perfusion
Staining and Labeling
Oxygen

Keywords

  • Carbon dioxide
  • Hypercarbia
  • Oxygen-induced retinopathy
  • Rat
  • Retinopathy of prematurity

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems

Cite this

Carbon dioxide-induced retinopathy in the neonatal rat. / Holmes, Jonathan M; Zhang, Shuichen; Leske, David A.; Lanier, William L.

In: Current Eye Research, Vol. 17, No. 6, 1998, p. 608-616.

Research output: Contribution to journalArticle

Holmes, Jonathan M ; Zhang, Shuichen ; Leske, David A. ; Lanier, William L. / Carbon dioxide-induced retinopathy in the neonatal rat. In: Current Eye Research. 1998 ; Vol. 17, No. 6. pp. 608-616.
@article{a1621d17151d4a808fbaf3a4778f9bb4,
title = "Carbon dioxide-induced retinopathy in the neonatal rat",
abstract = "Purpose. Hypercarbia has been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of hypercarbia on the retinal vasculature of the neonatal rat to determine whether hypercarbia alone could induce preretinal neovascularization analogous to ROP. Methods. In a preliminary blood gas study, 8-11-day-old rats were exposed to specific levels of inspired O2 and either 0.2{\%} CO2 or 10{\%} CO2. Arterial blood gases were obtained, and a level of inspired O2 was determined that, when combined with inspired 10{\%} CO2 would produce a PaO2 equivalent to room air (pure hypercarbia). In the formal retinopathy study, 300 newborn rats raised in 12 expanded litters (n = 25 each) were exposed for 7 days to either room air, 10{\%} CO2 in 21{\%} O2 and nitrogen (high-inspired CO2 group) or 10{\%} CO2 in 12.5{\%} O2 and nitrogen (pure-hypercarbia group). Each type of exposure was followed by recovery in room air for 5 days. Animals were sacrificed on day 13 and retinae were analyzed, using fluores cein perfusion and ADPase staining techniques. Results. Neovascularization occurred in 19{\%} of rats in the high-inspired CO2 group, and 14{\%} of rats in the pure-hypercarbia group, compared to 0{\%} of rats exposed to room air alone (p = 0.001, Chi square). Conclusions. In the neonatal rat model, exposure to hypercarbia alone, followed by room air recovery, results in preretinal neovascularization similar to that seen in oxygen-induced retinopathy. Our results support the suggestion that hypercarbia may be a risk factor for retinopathy of prematurity.",
keywords = "Carbon dioxide, Hypercarbia, Oxygen-induced retinopathy, Rat, Retinopathy of prematurity",
author = "Holmes, {Jonathan M} and Shuichen Zhang and Leske, {David A.} and Lanier, {William L.}",
year = "1998",
doi = "10.1076/ceyr.17.6.608.5176",
language = "English (US)",
volume = "17",
pages = "608--616",
journal = "Current Eye Research",
issn = "0271-3683",
publisher = "Informa Healthcare",
number = "6",

}

TY - JOUR

T1 - Carbon dioxide-induced retinopathy in the neonatal rat

AU - Holmes, Jonathan M

AU - Zhang, Shuichen

AU - Leske, David A.

AU - Lanier, William L.

PY - 1998

Y1 - 1998

N2 - Purpose. Hypercarbia has been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of hypercarbia on the retinal vasculature of the neonatal rat to determine whether hypercarbia alone could induce preretinal neovascularization analogous to ROP. Methods. In a preliminary blood gas study, 8-11-day-old rats were exposed to specific levels of inspired O2 and either 0.2% CO2 or 10% CO2. Arterial blood gases were obtained, and a level of inspired O2 was determined that, when combined with inspired 10% CO2 would produce a PaO2 equivalent to room air (pure hypercarbia). In the formal retinopathy study, 300 newborn rats raised in 12 expanded litters (n = 25 each) were exposed for 7 days to either room air, 10% CO2 in 21% O2 and nitrogen (high-inspired CO2 group) or 10% CO2 in 12.5% O2 and nitrogen (pure-hypercarbia group). Each type of exposure was followed by recovery in room air for 5 days. Animals were sacrificed on day 13 and retinae were analyzed, using fluores cein perfusion and ADPase staining techniques. Results. Neovascularization occurred in 19% of rats in the high-inspired CO2 group, and 14% of rats in the pure-hypercarbia group, compared to 0% of rats exposed to room air alone (p = 0.001, Chi square). Conclusions. In the neonatal rat model, exposure to hypercarbia alone, followed by room air recovery, results in preretinal neovascularization similar to that seen in oxygen-induced retinopathy. Our results support the suggestion that hypercarbia may be a risk factor for retinopathy of prematurity.

AB - Purpose. Hypercarbia has been suggested as a risk factor for retinopathy of prematurity (ROP). We investigated the effect of hypercarbia on the retinal vasculature of the neonatal rat to determine whether hypercarbia alone could induce preretinal neovascularization analogous to ROP. Methods. In a preliminary blood gas study, 8-11-day-old rats were exposed to specific levels of inspired O2 and either 0.2% CO2 or 10% CO2. Arterial blood gases were obtained, and a level of inspired O2 was determined that, when combined with inspired 10% CO2 would produce a PaO2 equivalent to room air (pure hypercarbia). In the formal retinopathy study, 300 newborn rats raised in 12 expanded litters (n = 25 each) were exposed for 7 days to either room air, 10% CO2 in 21% O2 and nitrogen (high-inspired CO2 group) or 10% CO2 in 12.5% O2 and nitrogen (pure-hypercarbia group). Each type of exposure was followed by recovery in room air for 5 days. Animals were sacrificed on day 13 and retinae were analyzed, using fluores cein perfusion and ADPase staining techniques. Results. Neovascularization occurred in 19% of rats in the high-inspired CO2 group, and 14% of rats in the pure-hypercarbia group, compared to 0% of rats exposed to room air alone (p = 0.001, Chi square). Conclusions. In the neonatal rat model, exposure to hypercarbia alone, followed by room air recovery, results in preretinal neovascularization similar to that seen in oxygen-induced retinopathy. Our results support the suggestion that hypercarbia may be a risk factor for retinopathy of prematurity.

KW - Carbon dioxide

KW - Hypercarbia

KW - Oxygen-induced retinopathy

KW - Rat

KW - Retinopathy of prematurity

UR - http://www.scopus.com/inward/record.url?scp=0031809337&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031809337&partnerID=8YFLogxK

U2 - 10.1076/ceyr.17.6.608.5176

DO - 10.1076/ceyr.17.6.608.5176

M3 - Article

VL - 17

SP - 608

EP - 616

JO - Current Eye Research

JF - Current Eye Research

SN - 0271-3683

IS - 6

ER -