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In Vivo Vascular Injury Readouts in Mouse Retina to Promote Reproducibility
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[Time-resolved autofluorescence in retinal vascular occlusions].

D Schweitzer1, S Quick, M Klemm

  • 1Bereich Experimentelle Ophthalmologie, Augenklinik der FSU Jena, Bachstraße 18, Jena, Germany. Dietrich.schweitzer@med.uni-jena.de

Der Ophthalmologe : Zeitschrift Der Deutschen Ophthalmologischen Gesellschaft
|June 17, 2010
PubMed
Summary

Time-resolved autofluorescence reveals metabolic changes in ocular tissue during branch retinal artery occlusion. NADH accumulation in undersupplied tissue significantly alters fluorescence lifetimes, indicating altered cellular metabolism.

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Area of Science:

  • Ophthalmology
  • Biophysics
  • Cellular Metabolism

Background:

  • Cellular metabolism assessment via time-resolved autofluorescence.
  • Ocular tissue fluorescence is a complex mix of endogenous fluorophores.
  • Branch retinal artery occlusion provides a model for comparing metabolic changes in diseased versus healthy ocular tissue.

Observation:

  • Time-resolved autofluorescence measured in two spectral channels (K1: 490-560 nm, K2: 560-700 nm).
  • Measurements compared between patients with branch retinal artery occlusion and healthy controls.
  • Fluorescence decay curves were approximated using a 3-exponential model.

Findings:

  • In K1, a reduced lifetime (τ1) was observed in undersupplied tissue, while τ2 was significantly elongated compared to healthy tissue.

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  • In K2, τ2 distribution was similar between healthy and undersupplied tissues.
  • Healthy ocular tissue exhibited a uniform distribution of fluorescence lifetimes across fundus regions.

    • Implications:

    • Elongation of τ1 in undersupplied tissue suggests a reduced contribution from protein-bound flavin adenine dinucleotide (FAD).
    • Significant elongation of τ2 (approx. 1.5 ns vs. 500 ps) in undersupplied tissue is likely due to increased protein-bound nicotinamide adenine dinucleotide (NADH) from glycolysis.
    • These findings highlight altered metabolic pathways, specifically glycolysis, in response to ischemic events in the retina.