May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Oxygen–Induced Retinopathy in Neonatal Rats: How Much Oxygen Do We Need?
Author Affiliations & Notes
  • Z. Charara
    Dép. de biologie, Université de Montréal, Montreal, PQ, Canada
  • A.L. Dorfman
    Pharmacology and Therapeutics,
    McGill University/Montreal Children's Hospital, Montreal, PQ, Canada
  • S. Joly
    Dép. de biologie, Université de Montréal, Montreal, PQ, Canada
  • J. Racine
    Ophthalmology/Neurology–Neurosurgery,
    McGill University/Montreal Children's Hospital, Montreal, PQ, Canada
  • S. Chemtob
    Pharmacology and Therapeutics, McGill University, Montreal, PQ, Canada
  • P. Lachapelle
    Ophthalmology/Neurology–Neurosurgery,
    McGill University/Montreal Children's Hospital, Montreal, PQ, Canada
  • Footnotes
    Commercial Relationships  Z. Charara, None; A.L. Dorfman, None; S. Joly, None; J. Racine, None; S. Chemtob, None; P. Lachapelle, None.
  • Footnotes
    Support  CIHR and Réseau Vision
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3440. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Z. Charara, A.L. Dorfman, S. Joly, J. Racine, S. Chemtob, P. Lachapelle; Oxygen–Induced Retinopathy in Neonatal Rats: How Much Oxygen Do We Need? . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3440.

      Download citation file:


      © ARVO (1962-2015); The Authors (2016-present)

      ×
  • Supplements
Abstract

Abstract: : Purpose: Previous studies have shown that the retina of newborn pigmented Long Evans (LE) rats and albino Sprague Dawley (SD) rats exposed to hyperoxia (80% O2) during the second week of life sustain permanent functional and structural damage. The purpose of this study was to find the threshold at which exposure to hyperoxia causes this damage. Methods: Newborn LE (n=35) and SD rats (n=45) were exposed to hyperoxia (40%, 60% and 80%) from birth to postnatal day six and 14, respectively and from postnatal day 6 through 14. Results were compared to control rats raised in room air. Scotopic (intensity: –6.3 to 0.6 log cd.m–2.s; 12 hours dark adaptation) and photopic (intensity: 0.9 log cd.m–2.s, background: 30 cd.m–2) ERGs were recorded at postnatal days 30 and 60. Retinal sections (enucleation at 60 days; 0.5 µm sections, toluidine blue staining) were also analyzed in rats exposed from day 0 to day 14. Results: A typical and predictable (based on a dose–response effect) oxygen induced retinopathy could be evidenced following 60% O2 exposure in SD and LE rats. In contrast, exposure to 40% O2 had no significant detrimental effect on the photopic and scotopic responses of SD rats, while LE rats showed a significant reduction in photopic and scotopic ERG amplitudes following exposure between P6–P14 only. Histological analysis revealed a thinning of the ONL, INL and IPL for LE rats exposed to 40%, 60% and 80% O2, as well as a thinning of the OPL at 40% and a complete destruction of the latter following exposures to 60% and 80% O2. Conclusions:Exposure to 40% O2 is not sufficient to bring about significant functional or structural changes in SD rats, whereas LE rats are already affected at this concentration. Our results would therefore further support our previous demonstration that LE rats are more susceptible than SD rats to postnatal hyperoxia. The reasons for this strain difference remains to be elucidated.

Keywords: retinopathy of prematurity • electroretinography: non-clinical • oxidation/oxidative or free radical damage 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×