May 2008
Volume 49, Issue 13
ARVO Annual Meeting Abstract  |   May 2008
Non-Invasive Fluorescence Anisotropy Imaging in Living Humans Eyes Agrees With Invasive Oxygen Microelectrode Data in Non-Human Primates
Author Affiliations & Notes
  • R. Zuckerman
    Biometric Imaging Inc, Philadelphia, Pennsylvania
  • Footnotes
    Commercial Relationships  R. Zuckerman, Biometric Imaging, Inc., E; Ralph Zuckerman, P.
  • Footnotes
    Support  Harris Methodist Health Foundation
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 6124. doi:
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      R. Zuckerman; Non-Invasive Fluorescence Anisotropy Imaging in Living Humans Eyes Agrees With Invasive Oxygen Microelectrode Data in Non-Human Primates. Invest. Ophthalmol. Vis. Sci. 2008;49(13):6124. doi:

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

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Purpose: : Fluorescence anisotropy imaging (Biometric Imaging Metabolic Mapper (Zuckerman et al., IOVS, 46: 4759, 2005; Zuckerman, IOVS, 47: 3344, 2006) is the first imaging modality to allow non-invasive imaging of mitochondrial function in the living human eye in 3-D space. To confirm that our novel method measures oxidative metabolism we mapped fluorescence anisotropy in normal human volunteers under conditions that precisely replicated those used in invasive oxygen microelectrode experiments on non-human primates. Moreover, metabolic mapping, unlike invasive oxygen microelectrodes, measures retinal metabolism at hundreds of thousands of points in space in <100 msec, and can access the inner retina for the first time.

Methods: : Steady-state fluorescence anisotropy mapping was performed under the following conditions: (1) dark adapted and light adapted states (≈ 1000 photons/rod/sec), (2) conditions of hyperoxia and normoxia, and (3) conditions of flickered light stimulation to drive inner retinal cells across a field that included the temporal retina and optic nerve head (ONH). Since anisotropies are additive we separated outer from inner retinal contributions by subtracting dark-adapted maps from light adapted ones both under steady-state illumination and during flicker.

Results: : Measurements of the time course of fluorescence anisotropy change to light stimulation revealed that metabolism lagged behind photovoltages with a latency of ≈ 2 sec, consistent with oxygen microelectrode determinations, thus confirming that measurements made within 100 msec reflect the dark-adapted state. Steady-state light stimulation decreased metabolism in rod rich regions by 43.1 +/- 6% (P<0.0001). Under normoxic conditions parafoveal metabolism exceeded that of foveal metabolism and 100% O2 inspiration by nasal tube increased parafoveal metabolism by 10.1 +/- 1.5% (P<0.0001) while foveal metabolism remained unchanged (P=0.887). At the ONH hyperoxia increased metabolism only at the neuroretinal rim, while increasing metabolism in regions surrounding the ONH. Subtraction of dark adapted maps from those acquired during flickered light revealed the inner retinal response to flicker.

Conclusions: : Non-invasive fluorescence anisotropy mapping in humans very closely corresponded to oxidative metabolism determined by invasive microelectrodes in non-human primates under all conditions studied. Our novel method provides the first means of studying retinal metabolism and neural processing in living human eyes in both health and disease in 3-D space. Effects of disease will be presented.

Keywords: imaging/image analysis: non-clinical • metabolism • retina 

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