April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Bright Light Exposure also Triggers a Vasculopathy
Author Affiliations & Notes
  • Anna Polosa
    Ophthalmology/Neurology-Neurosurgery, McGill Univ/Montreal Children's Hospital, Montreal, Quebec, Canada
  • Allison L. Dorfman
    Ophthalmology/Neurology-Neurosurgery, McGill Univ/Montreal Children's Hospital, Montreal, Quebec, Canada
  • Pierre Lachapelle
    Ophthalmology/Neurology-Neurosurgery, McGill Univ/Montreal Children's Hospital, Montreal, Quebec, Canada
  • Footnotes
    Commercial Relationships  Anna Polosa, None; Allison L. Dorfman, None; Pierre Lachapelle, None
  • Footnotes
    Support  Réseau Vision and NSERC
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1380. doi:
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      Anna Polosa, Allison L. Dorfman, Pierre Lachapelle; Bright Light Exposure also Triggers a Vasculopathy. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1380.

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

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Abstract

Purpose: : We have previously shown that the juvenile rat model of light-induced retinopathy (LIR) is characterized by severe and irreversible functional (flash and multifocal ERGs [fERG and mfERG]) and structural (retinal histology) features that are reminiscent of the human atrophic form of age-related macular degeneration (AMD) (ARVO 2010). The purpose of this study was to examine if LIR also had a vascular component.

Methods: : Sprague Dawley (SD) rats were exposed to a bright environment (10,000 lux) from P14-28 (juveniles, [J], n=6) or for 6 consecutive days (adults, [A], n=4), following which retinal flatmounts were prepared and stained with Isolectin (1:100) after 1, 30 or 100 days post-exposure, respectively. Retinas were divided into superior, inferior, nasal and temporal quadrants for analysis of retinal vasculature, where each quadrant was reconstructed by a series of 13 sequential overlapping images. Vascular density analysis obtained from LIR groups were compared with that from control (n=7), for which values were set at 100%.

Results: : Control J and A retinas revealed a similar vascular density (61.0±2.7%) which was consistently observed throughout each quadrant. One day following bright light exposure, however, retinal density was already significantly attenuated to approximately 35.0±2.2% and 30.4±6.7% in J and A groups, respectively (p<0.05), and these values did not change with time [J (D100): 28.2±2.5% and A (D30): 25.3±3.5%; p>0.05] or with retinal quadrants.

Conclusions: : Our results show that LIR is characterized by a significant vasculopathy in addition to the damage at the retinal ultrastructure (ONL thickness) and function (ERG attenuation) previously reported. However, this vasculopathy is maximal as soon as the exposure ends, that is long before the ONL and ERG consequences of LIR are measurable. Furthermore, unlike ONL and ERG findings, the vasculopathy does not appear to progress over time or show retinal quadrant disparity. Results would thus suggest that the LIR vasculopathy either develops concomitantly with the LIR retinopathy or triggers it. One wonders whether the prevention of this light induced vasculopathy could have a protective effect against the outcomes of LIR. Funded by Réseau Vision and NSERC.

Keywords: retina • radiation damage: light/UV 
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