Abstract

A theoretical model examining the effects of erythrocyte oxygenation on optoacoustic (OA) signals is presented. Each erythrocyte is considered as a fluid sphere and its optical absorption is defined by its oxygen saturation state. The OA field generated by a cell is computed by solving the wave equation in the frequency domain with appropriate boundary conditions. The resultant field from many cells is simulated by summing the pressure waves emitted by individual cells. A Monte Carlo algorithm generates 2-D spatially random distributions of oxygenated and deoxygenated erythrocytes. Oxygen saturation levels of oxygenated cells a assumed to be 100% and 0% for deoxygenated cells. The OA signal amplitude decreases monotonically for the 700-nm laser source and increases monotonically for 1000 nm optical radiation when blood oxygen saturation varies from 0 to 100%. An approximately sixfold decrease and fivefold increase of the OA signal amplitude were computed at those wavelengths, respectively. The OA spectral power in the low-frequency range (<10 MHz) and in the very high-frequency range (>100 MHz) decreases for 700 nm and increases for 1000 nm with increasing blood oxygen saturation. This model provides a theoretical framework to study the erythrocyte oxygenation-dependent OA signals.

Highlights

  • A theoretical model examining the effects of erythrocyte oxygenation on optoacoustic (OA) signals is presented

  • A number of experimental studies have been performed to investigate the potential of the OA technique to monitor blood oxygenation

  • The 2-D sample was assumed to be occupied by a collection of spatially random distribution of red blood cell (RBC) at a 45%

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Summary

Introduction

A theoretical model examining the effects of erythrocyte oxygenation on optoacoustic (OA) signals is presented. The OA field generated by a cell is computed by solving the wave equation in the frequency domain with appropriate boundary conditions. The OA signal amplitude decreases monotonically for the 700-nm laser source and increases monotonically for 1000 nm optical radiation when blood oxygen saturation varies from 0 to 100%. The OA spectral power in the low-frequency range (100 MHz) decreases for 700 nm and increases for 1000 nm with increasing blood oxygen saturation. This model provides a theoretical framework to study the erythrocyte oxygenation-dependent. Esenaliev et al.[11] carried out an in vitro experimental work and showed that OA signal amplitude increased monotonically with blood oxygenation when probed using a

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