Rejection of transplanted hearts remains an important reason for death of transplanted children. Finding diagnostic tools
for its detection can therefore improve the prognosis in this population of patients. Endomyocardial biopsy (EMB) by
cardiac catheterization is currently accepted as the "gold standard" for the diagnosis of rejection. Here, we investigate
new approach to monitor mitochondrial metabolic state of cardiac cells using spectrally-resolved autofluorescence
lifetime detection of nicotinamide adenine dinucleotide (phosphate), or NAD(P)H, the principal electron donor in
mitochondrial oxidative energy metabolism responsible for vital ATP supply of cardiomyocytes. NAD(P)H
autofluorescence is long used for non-invasive fluorescent probing the metabolic state of the heart. In this contribution
we report dynamic characteristics of NAD(P)H fluorescence decays in living human cardiomyocytes from EMB,
following excitation by UV-pulsed laser diode and detection by spectrally-resolved time-correlated single photon
counting. At least a 3-exponential decay model, with 0.5-0.7 ns, 1.9-2.4 ns and 9.0-15.0 ns lifetimes, is necessary to
describe cardiomyocyte autofluorescence in human cells. When gathered data were compared to those recorded under
same conditions in rats, autofluorescence in human hearts was found significantly lower in comparison to rat ones.
Rotenone, the inhibitor of the Complex I of the respiratory chain, increased the fluorescence in human cardiac cells,
making them more comparable to experimental rat model. These results suggest that human cardiac cells are more
metabolically active than the rat ones in the same conditions. Presented work proposes a new tool for evaluation of
oxidative metabolism changes in transplanted hearts.