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Zeitaufgelöste Autofluoreszenz bei retinalen Gefäßverschlüssen

Time-resolved autofluorescence in retinal vascular occlusions

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Zusammenfassung

Hintergrund

Der zelluläre Metabolismus kann mittels zeitaufgelöster Autofluoreszenz (FLIM) beurteilt werden. Die Überlagerung verschiedener endogener Fluorophore in okulären Geweben erschwert Aussagen zu einzelnen Fluorophoren. Bei Verschlüssen retinaler Astarterien können lokale Änderungen des Stoffwechsels mit gesundem Gewebe verglichen werden.

Methode

FLIM von 2 Patienten wurde in 2 Spektralkanälen K1 (490–560 nm), K2 (560–700 nm) gemessen, triexponentiell approximiert und mit repräsentativen Ergebnisse eines gesunden Auges verglichen.

Ergebnisse

In K1 war die Lebensdauer τ1 im unterversorgten Gewebe leicht, τ2 jedoch stark gegenüber dem gesunden Gewebe verlängert. In K2 waren die Verteilungen von τ2 deckungsgleich in beiden Geweben. Am gesunden Auge waren die Verteilungen aller Lebensdauern identisch zwischen entsprechenden Fundusgebieten.

Schlussfolgerung

Die Verlängerung von τ1 im unterversorgten Gewebe ist auf geringeren Beitrag von proteingebundenem FAD zurückzuführen. Die Verlängerung von τ2 (ca. 500 ps) in gesundem Gewebe gegenüber ca. 1, 5 ns im unterversorgten ist wahrscheinlich durch proteingebundenes NADH verursacht, das bei der Glykolyse entsteht.

Abstract

Background

Cellular metabolism can be evaluated using time-resolved autofluorescence. Because the fluorescence of ocular tissue is an accumulation of the fluorescence of several endogenous fluorophores, it is hard to determine the influence of a single fluorophore. In branch retinal artery occlusion, metabolic changes can be compared with normal tissue.

Method

Time-resolved autofluorescence was measured in two patients in two spectral channels, K1 (490–560 nm) and K2 (560–700 nm), and was 3-exponentially approximated and compared with representative results of a healthy eye.

Results

In K1, lifetime τ1 in the undersupplied tissue was weak, but τ2 was strongly elongated compared with the healthy tissue. In K2, the distribution of τ2 was identical in both tissues. In the healthy eye, there was an equal distribution of all lifetimes in corresponding fundus regions.

Conclusions

The elongation of τ1 in undersupplied tissue is probably caused by a reduced contribution of protein-bound FAD. The elongation of τ2 (about 500 ps) in healthy tissue, compared to about 1.5 ns in undersupplied tissue, is probably caused by protein-bound NADH, which is formed in glycolysis.

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Interessenskonflikt

Der Beitrag wurde in Teilen zur Tagung der Deutschen Ophthalmologischen Gesellschaft 2009 vorgetragen.

Der Aufbau des Demonstrators wurde von Heidelberg Engineering im Rahmen eines industriegeförderten Drittmittelprojekts unterstützt.

Die Autoren hatten kein finanzielles Interesse an der Ausführung der Studie.

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Authors and Affiliations

  1. Bereich Experimentelle Ophthalmologie, Augenklinik der FSU Jena, Bachstraße 18, 07743, Jena, Deutschland

    D. Schweitzer, S. Quick, M. Hammer, S. Jentsch & J. Dawczynski

  2. Institut für Biomedizinische Technik und Informatik, Technische Universität Ilmenau, Ilmenau, Deutschland

    M. Klemm

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  1. D. Schweitzer
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  2. S. Quick
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  3. M. Klemm
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  4. M. Hammer
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  5. S. Jentsch
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  6. J. Dawczynski
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Correspondence to D. Schweitzer.

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Schweitzer, D., Quick, S., Klemm, M. et al. Zeitaufgelöste Autofluoreszenz bei retinalen Gefäßverschlüssen. Ophthalmologe 107, 1145–1152 (2010). https://doi.org/10.1007/s00347-010-2195-7

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  • DOI: https://doi.org/10.1007/s00347-010-2195-7

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