May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
The Efficacy of Delayed Oxygen Therapy Following Experimental Retinal Detachment
Author Affiliations & Notes
  • G.P. Lewis
    Neuroscience Research Inst, Univ of CA Santa Barbara, Santa Barbara, CA, United States
  • K.A. Linberg
    Neuroscience Research Inst, Univ of CA Santa Barbara, Santa Barbara, CA, United States
  • K.C. Talaga
    Neuroscience Research Inst, Univ of CA Santa Barbara, Santa Barbara, CA, United States
  • R.L. Avery
    Neuroscience Research Inst, Univ of CA Santa Barbara, Santa Barbara, CA, United States
  • S.K. Fisher
    Neuroscience Research Inst and MCD Biology, Univ of CA Santa Barbara, Santa Barbara, CA, United States
  • Footnotes
    Commercial Relationships  G.P. Lewis, None; K.A. Linberg, None; K.C. Talaga, None; R.L. Avery, None; S.K. Fisher, None.
  • Footnotes
    Support  NIH Grant EY00888 and a grant from Santa Barbara Cottage Hospital, Santa Barbara CA
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2952. doi:
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      G.P. Lewis, K.A. Linberg, K.C. Talaga, R.L. Avery, S.K. Fisher; The Efficacy of Delayed Oxygen Therapy Following Experimental Retinal Detachment . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2952.

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

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Abstract

Abstract: : Purpose: Increasing environmental oxygen to 70% immediately after the production of a retinal detachment (RD) has been shown to prevent photoreceptor deconstruction and glial reactivity (Mervin et al., Lewis et al., AJO, 128, 1999). The purpose of this study was to determine the effect of delaying the hyperoxia by 24 hr after detachment. Methods: Experimental RDs were created in the right eye of domestic cats (n=8). All animals remained in room air for 24 hr at which time 4 were placed in an environment with the oxygen concentration held precisely at 70% by an "Oxycycler" feedback control device (BioSpherix, Redfield, NY). Seven days after the creation of the retinal detachment, half of each eye was prepared for morphological analysis and the other half for immunohistochemistry. The TUNEL assay was used to detect apoptotic cells and the MIB-1 antibody was used to detect dividing cells. Results: Labeling with rod and cone opsin antibodies as well as with probes to the interphotoreceptor matrix (the lectin PNA and anti-chondroitin sulfate) showed that the outer segments (OS) and the matrix associated with them were dramatically preserved by hyperoxia even though treatment was delayed by 24 hr. Although there was some variability, little OS shortening or opsin redistribution was observed in the treated animals. They also showed a more normal distribution of mitochondria in photoreceptors (anti-cytochrome oxidase), less rod synaptic terminal retraction (anti-synaptophysin), and less neurite outgrowth from second order neurons (anti-PKC and -neurofilament). The labeling patterns of Mueller cells for glutamine synthetase, carbonic anhydrase II and cellullar retinaldehyde binding protein were similar to those in normal control eyes, but overall, Mueller cell reactivity, as indicated by anti-GFAP and -vimentin labeling, was not slowed by the increased oxygen. In addition, there was no difference in numbers of dividing cells or TUNEL labeled photoreceptor cells between control and hyperoxia treated animals. Conclusions: The results indicate that elevated oxygen, given 24 hr after a retinal detachment occurs, is effective at maintaining OS length, protein distribution, and synaptic terminals of rods and cones during a 7 day detachment period. However, the Mueller cell hypertrophy inititated during the 24 hr in room air, was not obviously slowed nor reversed by delayed oxygen therapy. Finally, elevated oxygen, given for a period of 6 days did not produce any obvious deleterious effects on the retina.

Keywords: retinal detachment • neuroprotection • photoreceptors 
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