Key result
A proposed haemodynamic model suggests that asynchronous contributions from arterial, capillary, and venous compartments may cause out-of-phase oscillations of oxy- and deoxyhaemoglobin in tissue.
This theoretical model provides a framework for interpreting in vivo haemodynamic and oximetric data from techniques like optical imaging and fMRI.
May inform NIRS/fMRI signal interpretation; leaves open empirical validation before clinical use.
We present a model that describes the effect of physiological parameters such as the speed of blood flow, local oxygen consumption, capillary recruitment, and vascular dilation/constriction on the concentration and oxygen saturation of haemoglobin in tissue. This model can be used to guide the physiological interpretation of haemodynamic and oximetric data collected in vivo with techniques such as optical imaging, near-infrared spectroscopy and functional magnetic resonance imaging. In addition to providing a formal description of well-established results (exercise-induced hyperemia, reperfusion hyperoxia, decrease in the concentration of deoxyhaemoglobin induced by brain activity, measurement of arterial saturation by pulse oximetry, etc.), this model suggests that the superposition of asynchronous contributions from the arterial, capillary and venous haemoglobin compartments may be at the origin of observed out-of-phase oscillations of the oxyhaemoglobin and deoxyhaemoglobin concentrations in tissue.
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Sergio Fantini (2002) studied this question. Haemodynamic model was evaluated. A proposed haemodynamic model suggests that asynchronous contributions from arterial, capillary, and venous compartments may cause out-of-phase oscillations of oxy- and deoxyhaemoglobin in tissue.
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