September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Inner retinal oxygen delivery and metabolism following ischemia/reperfusion injury in rat
Author Affiliations & Notes
  • Michael Robert Tan
    Opthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States
  • Anthony E Felder
    Opthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States
  • Justin Wanek
    Opthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States
  • Norman P Blair
    Opthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States
  • Mahnaz Shahidi
    Opthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, Illinois, United States
  • Footnotes
    Commercial Relationships   Michael Tan, None; Anthony Felder, None; Justin Wanek, None; Norman Blair, None; Mahnaz Shahidi, US8332007 B2 (P)
  • Footnotes
    Support  NIH Grants EY017918 and EY001792, and Research to Prevent Blindness
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 2206. doi:
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    • Get Citation

      Michael Robert Tan, Anthony E Felder, Justin Wanek, Norman P Blair, Mahnaz Shahidi; Inner retinal oxygen delivery and metabolism following ischemia/reperfusion injury in rat. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2206.

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

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Abstract

Purpose : The purpose of this study is to report measurements of inner retinal oxygen delivery (DO2) and metabolism (MO2) following retinal ischemia/reperfusion (I/R) injury in rat.

Methods : One eye of each rat (N=4) was subjected to acute ischemia by cannulation of the anterior chamber to elevate intraocular pressure (IOP) for 90 minutes. The fellow eye was not cannulated and served as control. Retinal vascular oxygen tension (PO2) and blood flow imaging were performed one or two weeks following cannulation. PO2 was measured in major retinal arteries (PO2A) and veins (PO2V) by phosphorescence lifetime section imaging. Arterial and venous oxygen contents (O2A and O2V, respectively) were calculated from these measurements using the rat oxygen-hemoglobin dissociation curve. Velocity and diameter were measured in retinal veins by fluorescent microsphere and red-free retinal imaging, respectively allowing total venous blood flow (F) calculation. DO2 and MO2 were calculated as F*O2A and F*(O2A - O2V), respectively. Oxygen extraction fraction (OEF) was calculated as a ratio of MO2 and DO2. Data were analyzed using paired t-tests.

Results : Prior to cannulation, IOP in study and fellow eyes were 10±0.6 mmHg and 10±0.4 mmHg, respectively. IOP in study eyes during cannulation (63±11 mmHg) was significantly elevated compared to fellow eyes (P<0.001). During imaging, IOP was 10±1 mmHg and 11±1 mmHg in study and fellow eyes, respectively. PO2A and O2A were decreased in study eyes as compared to fellow eyes (P<0.004), while PO2V and O2v were not significantly different (P≥0.05). F decreased significantly in study eyes compared to fellow eyes (P=0.04). DO2 in study eyes (969±168 nL O2/min) was decreased compared to fellow eyes (1457±84 nL O2/min) (P=0.02). Likewise, MO2 in study eyes (457±86 nL O2/min) was decreased compared to fellow eyes (619±80 nL O2/min) (P=0.003). OEF was not significantly different between study (0.48±0.07) and fellow (0.43±0.05) eyes (P=0.2).

Conclusions : DO2 and MO2 were quantified for the first time following retinal ischemia/reperfusion injury in rats and were reduced, suggesting retinal cell loss, a diminished need for energy production and compensation by retinal vasculature to maintain OEF. These findings may have implications for understanding the pathophysiology of retinal ischemic conditions.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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