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WIREs Syst Biol Med
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Integration of cardiovascular regulation by the blood/endothelium cell‐free layer

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Abstract The cell‐free layer (CFL) width separating red blood cells in flowing blood from the endothelial cell membrane is shown to be a regulator of the balance between nitric oxide (NO) production by the endothelium and NO scavenging by blood hemoglobin. The CFL width is determined by hematocrit (Hct) and the vessel wall flow velocity gradient. These factors and blood and plasma viscosity determine vessel wall shear stress which regulates the production of NO in the vascular wall. Mathematical modeling and experimental findings show that vessel wall NO concentration is a strong nonlinear function of Hct and that small Hct variations have comparatively large effects on blood pressure regulation. Furthermore, NO concentration is a regulator of inflammation and oxygen metabolism. Therefore, small, sustained perturbations of Hct may have long‐term effects that can promote pro‐hypertensive and pro‐inflammatory conditions. In this context, Hct and its variability are directly related to vascular tone, peripheral vascular resistance, oxygen transport and delivery, and inflammation. These effects are relevant to the analysis and understanding of blood pressure regulation, as NO bioavailability regulates the contractile state of blood vessels. Furthermore, regulation of the CFL is a direct function of blood composition therefore understanding of its physiology relates to the design and management of fluid resuscitation fluids. From a medical perspective, these studies propose that it should be of clinical interest to note small variations in patient's Hct levels given their importance in modulating the CFL width and therefore NO bioavailability. WIREs Syst Biol Med 2011 3 458–470 DOI: 10.1002/wsbm.150 This article is categorized under: Physiology > Mammalian Physiology in Health and Disease

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Diagrammatic representation of the compartments at the blood tissue interface drawn approximately to scale during flow.

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Changes in blood pressure and cardiac output due to small changes in Hct according to the experimental results of Martini et al.78,80 and Salazar Vásquez et al.81 The data is presented as a function of the change in Hct and the corresponding changes in plasma layer width in arterioles according to the results of Yalcin et al.82

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Cell‐free plasma layer (CFL) in vivo. Image of an arteriolar wall showing CFL width, the distance between the RBC column (black), and the endothelium lining the vessel wall. This image shows a few red blood cells (RBCs) positioned closer to the endothelium. CFL width is the distance between A and B, or the difference between the radius of the inner endothelial surface Re and radius of the RBC column RRBC. The RBCs are 7 µm in diameter. Blood flow is from right to left (arrow).

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