May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Imaging of Chorio–retinal Oxygenation in Experimental Carotid Occlusion.
Author Affiliations & Notes
  • M. Shahidi
    Ophthalmology & Visual Sciences, University of Illinois at Chicago, Chicago, IL
  • N.P. Blair
    Ophthalmology & Visual Sciences, University of Illinois at Chicago, Chicago, IL
  • A. Shakoor
    Ophthalmology & Visual Sciences, University of Illinois at Chicago, Chicago, IL
  • M. Mori
    Ophthalmology & Visual Sciences, University of Illinois at Chicago, Chicago, IL
  • Footnotes
    Commercial Relationships  M. Shahidi, None; N.P. Blair, None; A. Shakoor, None; M. Mori, None.
  • Footnotes
    Support  NIH grant EY14917
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2410. doi:
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      M. Shahidi, N.P. Blair, A. Shakoor, M. Mori; Imaging of Chorio–retinal Oxygenation in Experimental Carotid Occlusion. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2410.

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

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Abstract

Abstract: : Purpose: To study experimentally induced retinal hypoxia with the use of an optical system that was established for noninvasive imaging of oxygenation in the chorio–retinal vasculatures. Methods: Imaging of the choroi–retinal oxygenation was performed by projecting a narrow laser line at an angle on the retina after intravenous injection of an oxygen–sensitive probe (Pd porphine) and viewing phosphorescence emission. A phosphorescence optical section image of the retina was captured allowing separate imaging of oxygenation in the choroi–retinal vasculatures simultaneously. Imaging was performed in three rats, under normal resting condition and following temporary occlusion of the common carotid artery to induce retinal hypoxia. The digital optical section images were analyzed and the average phosphorescence intensity in a retinal vein (Iv), a retinal artery (Ia), choroid (Ic), and retinal microvasculature (Im) were separately measured. The percent change in phosphorescence intensity, signifying the change in oxygenation, was determined from the measurements obtained before (initial) and following (final) occlusion [I(final) – I(initial)/I(initial)]*100. Results: Under resting condition, the intensity of the probe phosphorescence remained essentially constant. The changes in Iv, Ia, Ic and Im over time were 2 + 2%, –1 + 4%, 1 + 2%, and 6 + 3%, respectively. Following occlusion, the intensity of the probe phosphorescence increased, indicating a decrease in the oxygenation in the chorio–retinal vasculatures and experimentally induced temporary retinal hypoxia. Within 15 + 5 sec (mean + SD) of occlusion, the maximum changes in Iv, Ia, Ic and Im were found to be 50 + 6%, 12 + 3%, 7 + 8%, and 23 + 21%, respectively. The phosphorescence intensity returned to the resting condition values with reversal of occlusion, indicating re–oxygenation of retinal tissue after reperfusion. Conclusion: The results demonstrate the feasibility of our noninvasive imaging technique for studying experimentally–induced retinal hypoxia and understanding disease–related oxygen dynamics separately in retinal, choroidal, and intra–retinal vasculatures.

Keywords: imaging methods (CT, FA, ICG, MRI, OCT, RTA, SLO, ultrasound) • imaging/image analysis: non–clinical • hypoxia 
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