June 2020
Volume 61, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2020
Retinal Oxygen Metabolism and Delivery Response to Hyperoxia During Bilateral Common Carotid Artery Occlusion in Rats
Author Affiliations & Notes
  • Sophie Leahy
    University of Southern California, Los Angeles, California, United States
  • Nathanael Matei
    University of Southern California, Los Angeles, California, United States
  • Norman P Blair
    Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States
  • Mahnaz Shahidi
    University of Southern California, Los Angeles, California, United States
  • Footnotes
    Commercial Relationships   Sophie Leahy, None; Nathanael Matei, None; Norman Blair, None; Mahnaz Shahidi, University of Illinois at Chicago (P)
  • Footnotes
    Support  NIH research grant EY017918 and EY029220 and Research to Prevent Blindness
Investigative Ophthalmology & Visual Science June 2020, Vol.61, 182. doi:
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      Sophie Leahy, Nathanael Matei, Norman P Blair, Mahnaz Shahidi; Retinal Oxygen Metabolism and Delivery Response to Hyperoxia During Bilateral Common Carotid Artery Occlusion in Rats. Invest. Ophthalmol. Vis. Sci. 2020;61(7):182.

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

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Abstract

Purpose : Hyperoxia has been shown to diminish injury induced by ischemia. We previously reported reduced inner retinal oxygen metabolism (MO2) and delivery (DO2) as well as increased oxygen extraction fraction (OEF) after permanent bilateral common carotid artery occlusion (BCCAO). The effect of hyperoxia on these oxygen metrics has not been investigated. We hypothesized that hyperoxia improves MO2 and DO2 under ischemia induced by BCCAO in rats.

Methods : Thirteen rats underwent BCCAO and were imaged in one eye either immediately or 3 days later under both spontaneous breathing condition (normoxia) and 15 minutes of 100% O2 inspiration (hyperoxia). In 6 of these rats, baseline imaging was performed before BCCAO. Phosphorescence lifetime, microsphere fluorescence, and reflectance images were acquired to derive MO2, DO2, and OEF.

Results : MO2, DO2 and OEF were impaired immediately after BCCAO compared to baseline (P≤0.03; N=6). On average, MO2 and DO2 decreased to 52% and 19% of baseline values, respectively, and OEF increased to 301% of baseline value. Immediately after BCCAO, MO2 and DO2 increased under hyperoxia (220±96 and 260±140 nLO/min, respectively) compared to that under normoxia (120±82 and 120±83 nLO/min, respectively) (P≤0.04; N=9). OEF was not significantly different under hyperoxia (0.90±0.11) compared to that under normoxia (0.98±0.02) (P=0.06). MO2 and DO2 under normoxia were inversely correlated to changes in the corresponding measurement under hyperoxia (r≥0.88; P≤0.002; N=9). After 3 days of BCCAO, there were no significant differences in MO2, DO2, and OEF under normoxia (230±110 nLO/min, 300±81 nLO/min, and 0.74±0.16, respectively) compared to that under hyperoxia (170±51 nLO/min, 440±300 nLO/min, 0.53±0.31, respectively) (P≥0.17; N=4). MO2 and DO2 under normoxia were not correlated with changes in the corresponding measurement under hyperoxia (r≤0.91; P≥0.09; N=4).

Conclusions : MO2 and DO2 increased with hyperoxia immediately after BCCAO, and the increases were inversely related to their levels under normoxia. However, after 3 days of BCCAO, there was no detectable effect of hyperoxia on MO2 and DO2. OEF did not respond to hyperoxia at either time point. These results suggest that improvement in MO2 and DO2 by hyperoxia may be most effective shortly after ischemia, rather than after longer durations of ischemia.

This is a 2020 ARVO Annual Meeting abstract.

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