Wiley Interdiscip Rev Syst Biol Med - Integration of cardiovascular regulation by the blood/endothelium cell-free layer.

Tópicos

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Resumo

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

Resumo Limpo

cellfre layer cfl width separ red blood cell flow blood endotheli cell membran shown regul balanc nitric oxid product endothelium scaveng blood hemoglobin cfl width determin hematocrit hct vessel wall flow veloc gradient factor blood plasma viscos determin vessel wall shear stress regul product vascular wall mathemat model experiment find show vessel wall concentr strong nonlinear function hct small hct variat compar larg effect blood pressur regul furthermor concentr regul inflamm oxygen metabol therefor small sustain perturb hct may longterm effect can promot prohypertens proinflammatori condit context hct variabl direct relat vascular tone peripher vascular resist oxygen transport deliveri inflamm effect relev analysi understand blood pressur regul bioavail regul contractil state blood vessel furthermor regul cfl direct function blood composit therefor understand physiolog relat design manag fluid resuscit fluid medic perspect studi propos clinic interest note small variat patient hct level given import modul cfl width therefor bioavail wire syst biol med doi wsbm

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