May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Fluorescence Lifetime Imaging – a Diagnostic Tool for Metabolic Mapping
Author Affiliations & Notes
  • D. Schweitzer
    Experimental Ophthalmology, University of Jena, Jena, Germany
  • F. Schweitzer
    Experimental Ophthalmology, University of Jena, Jena, Germany
  • M. Hammer
    Experimental Ophthalmology, University of Jena, Jena, Germany
  • E.R. Gaillard
    Chemistry and Biochemistry, Northern Illinois University, DeKalb, IL
  • F. Schuett
    Ophthalmology, University of Heidelberg, Heidelberg, Germany
  • Footnotes
    Commercial Relationships  D. Schweitzer, None; F. Schweitzer, None; M. Hammer, None; E.R. Gaillard, None; F. Schuett, None.
  • Footnotes
    Support  German BMBF Grant 01EZ0309
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 2957. doi:
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    • Get Citation

      D. Schweitzer, F. Schweitzer, M. Hammer, E.R. Gaillard, F. Schuett; Fluorescence Lifetime Imaging – a Diagnostic Tool for Metabolic Mapping . Invest. Ophthalmol. Vis. Sci. 2004;45(13):2957.

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

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Abstract

Abstract: : Purpose: To detect influences of endogenous fluorophores, which can be used for characterisation of metabolism at the fundus in AMD, diabetes , and glaucoma. Methods: The time–resolved autofluorescence of the fundus was measured by a modified Laser Scanning Ophthalmoscope with a pulse laser in combination with time–correlated single photon counting technique for lifetime measurements. This technique was applied in investigation of 19 healthy subjects and 14 AMD patients. In 3 normals, the metabolism was provoked by respiration of 100% oxygen for 6 min.. Comparing measurements were performed on isolated substances and on cultures of retinal pigment epithelium. Besides lifetime images of the fundus, the presentation of lifetime pairs of tau 1–tau 2 in a corresponding diagram allows the discrimination of fluorophores and of anatomical structures. Results: After bi–exponential approximation of the fluorescence decay, in healthy subjects, the dominating shortest values of lifetime tau 1 were determined in the macula and the longest in the optic disc. The lifetime tau 2 did not exhibit strong differences corresponding to anatomical structures. The lifetime tau 1 increases with age in the macula. In AMD patients with artificial lens, the lifetime tau 1 was further increased outside the optic disc. In case of cataract, also the lifetime tau 2 was strongly increased. The respiration of oxygen leads to changes in fluorescence lifetime, proving also the detection of co–enzymes at the fundus. Comparing the macular lifetime clusters with human liopfuscin, only a partially overlap was determined between both young normals and AMD patients with lipofuscin, but a complete overlap was found for some older normals. Conclusions: Besides known fluorescence of lipofuscin and of connective tissue, the study of co–enzyme fluorescence are steps for evaluation of retinal metabolism.

Keywords: age–related macular degeneration • retinal degenerations: cell biology • metabolism 
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