Time-resolved autofluorescence in retinal vascular occlusions

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. 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. In K1, lifetime tau 1 in the undersupplied tissue was weak, but tau 2 was strongly elongated compared with the healthy tissue. In K2, the distribution of tau 2 was identical in both tissues. In the healthy eye, there was an equal distribution of all lifetimes in corresponding fundus regions. The elongation of tau 1 in undersupplied tissue is probably caused by a reduced contribution of protein-bound FAD. The elongation of tau 2 (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.