Abstract
Autofluorescence spectroscopy is a promising label-free approach to characterize biological samples with demonstrated potential to report structural and biochemical alterations in tissues in a number of clinical applications. We report a characterization of the ex vivo autofluorescence fingerprint of cardiac tissue, exploiting a Langendorff-perfused isolated rat heart model to induce physiological insults to the heart, with a view to understanding how metabolic alterations affect the autofluorescence signals. Changes in the autofluorescence intensity and lifetime signatures associated with reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) and flavin adenine dinucleotide (FAD) were characterized during oxygen- or glucose-depletion protocols. Results suggest that both NAD(P)H and FAD autofluorescence intensity and lifetime parameters are sensitive to changes in the metabolic state of the heart owing to oxygen deprivation. We also observed changes in NAD(P)H fluorescence intensity and FAD lifetime parameter on reperfusion of oxygen, which might provide information on reperfusion injury, and permanent tissue damage or changes to the tissue during recovery from oxygen deprivation. We found that changes in the autofluorescence signature following glucose-depletion are, in general, less pronounced, and most clearly visible in NAD(P)H related parameters. Overall, the results reported in this investigation can serve as baseline for future investigations of cardiac tissue involving autofluorescence measurements.
Highlights
Heart diseases including ischemia-reperfusion injury during acute myocardial infarction and chronic heart failure are characterized by complex functional and morphological alterations of the myocardium leading to structural and energetic dysfunction [1,2]
In a previous study [25], we reported the application of time-resolved autofluorescence spectroscopy to characterize the in vivo autofluorescence signature of cardiac tissue in a 16 week myocardial infarction heart failure rat model
We found an inconsistent response in flavin adenine dinucleotide (FAD) autofluorescence intensity in Channel 4: 1 out of 4 specimens showed an increase in autofluorescence during the insult; in the remaining 3 specimens the autofluorescence signal persisted relatively unchanged throughout the course of the experiments
Summary
Heart diseases including ischemia-reperfusion injury during acute myocardial infarction and chronic heart failure are characterized by complex functional and morphological alterations of the myocardium leading to structural and energetic dysfunction [1,2]. Advances in interventional and surgical techniques have allowed access to measurements of cardiac function using intracardiac electrodes, 3D echocardiography or pressure wires None of these approaches directly evaluates the viability of the myocardium itself, but rather the gross and late impairment in electrical and mechanical activity at the level of the whole ventricular chamber. NADH autofluorescence decay characteristics are commonly modelled with a bi-exponential function, where the short (τ1) and long (τ2) components refer to the free and protein-bound states of the molecule This interpretation has been questioned recently [21,22] by work suggesting that the change in NAD(P)H lifetime observed is affected by changes in NADPH fluorescence. In this paper we report the changes in the fluorescence decay parameters observed but avoid attributing these to specific biochemical changes
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