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.