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A theoretical model investigating the dependence of optoacoustic (OA) signal on blood oxygen saturation (SO(2)) is discussed. The derivations for the nonbandlimited and bandlimited OA signals from many red blood cells (RBCs) are presented. The OA field generated by many RBCs was obtained by summing the OA field emitted by each RBC approximated as a fluid sphere. A Monte Carlo technique was employed generating the spatial organizations of RBCs in two-dimensional. The RBCs were assumed to have the same SO(2) level in a simulated configuration. The fractional number of oxyhemoglobin molecules, confined in a cell, determined the cellular SO(2) and also defined the blood SO(2). For the nonbandlimited case, the OA signal amplitude decreased and increased linearly with blood SO(2) when illuminated by 700 and 1000 nm radiations, respectively. The power spectra exhibited similar trends over the entire frequency range (MHz to GHz). For the bandlimited case, three acoustic receivers with 2, 10, and 50 MHz as the center frequencies were considered. The linear variations of the OA amplitude with blood SO(2) were also observed for each receiver at those laser sources. The good agreement between simulated and published experimental results validates the model qualitatively.

Validity of a theoretical model to examine blood oxygenation dependent optoacoustics