Adequate oxygen delivery to a tissue depends on sufficient oxygen content in arterial blood and blood flow to the tissue. Oximetry is a technique for the assessment of blood oxygenation by measurements of light transmission through the blood, which is based on the different absorption spectra of oxygenated and deoxygenated hemoglobin. Oxygen saturation in arterial blood provides information on the adequacy of respiration and is routinely measured in clinical settings, utilizing pulse oximetry. Oxygen saturation, in venous blood (SvO2) and in the entire blood in a tissue (StO2), is related to the blood supply to the tissue, and several oximetric techniques have been developed for their assessment. SvO2 can be measured non-invasively in the fingers, making use of modified pulse oximetry, and in the retina, using the modified Beer–Lambert Law. StO2 is measured in peripheral muscle and cerebral tissue by means of various modes of near infrared spectroscopy (NIRS), utilizing the relative transparency of infrared light in muscle and cerebral tissue. The primary problem of oximetry is the discrimination between absorption by hemoglobin and scattering by tissue elements in the attenuation measurement, and the various techniques developed for isolating the absorption effect are presented in the current review, with their limitations.
Retinal hemodynamics plays a crucial role in the pathophysiology of several ocular diseases. There are clear evidences that the hemodynamics of the central retinal artery (CRA) is strongly affected by the level of intraocular pressure (IOP), which is the pressure inside the eye globe. However, the mechanisms through which this occurs are still elusive. The main goal of this paper is to develop a mathematical model that combines the mechanical action of IOP and the blood flow in the CRA to elucidate the mechanisms through which IOP elevation affects the CRA hemodynamics. Our model suggests that the development of radial compressive regions in the lamina cribrosa (a collagen structure in the optic nerve pierced by the CRA approximately in its center) might be responsible for the clinically-observed blood velocity reduction in the CRA following IOP elevation. The predictions of the mathematical model are in very good agreement with experimental and clinical data. Our model also identifies radius and thickness of the lamina cribrosa as major factors affecting the IOP-CRA relationship, suggesting that anatomical differences among individuals might lead to different hemodynamic responses to IOP elevation.
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