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Article type: Review Article
Authors: Salazar Vázquez, B.Y. | Martini, J. | Chávez Negrete, A. | Tsai, A.G. | Forconi, S. | Cabrales, P. | Johnson, P.C. | Intaglietta, M.;
Affiliations: Faculty of Medicine, Universidad Juárez del Estado de Durango, Victoria de Durango, DGO, Mexico | Department of Anesthesia and Intensive Care Medicine, Innsbruck Medical University, Innsbruck, Austria | Hospital de Especialidades, Instituto Mexicano de Seguro Social, México DF., Mexico | Department of Bioengineering, University of California, San Diego, CA, USA | Centro Siena–Toronto, University of Siena, Siena, Italy
Note: [] Corresponding author: Prof. M. Intaglietta, Department of Bioengineering – 0412, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA. E-mail: mintagli@ucsd.edu.
Abstract: Decreasing blood viscosity has been proposed since the advent of hemodilution as a means for increasing perfusion in many pathological conditions, and increased plasma viscosity is associated with the presence of pathological conditions. However, experimental studies show that microvascular functions as represented by functional capillary density in conditions of significantly decreased viscosity is impaired, a problem corrected by increasing plasma and blood viscosity. Blood viscosity, primarily dependent on hematocrit (Hct) is a determinant of peripheral vascular resistance, and therefore blood pressure. In the healthy population Hct presents a variability, which is not reflected by the variability of blood pressure. This is due to a regulatory process at the level of the endothelium, whereby the increase of Hct (and therefore blood viscosity) leads to increased shear stress and the production of the vasodilator nitric oxide (NO), a finding supported by experimental studies showing that the acute increase of Hct lowers blood pressure. Studies that in the healthy population show that blood pressure and Hct have a weak positive correlation. However, when the effect of blood viscosity is factored out, blood pressure and Hct are negatively and significantly correlated, indicating that as blood viscosity increases, the circulation dilates. Conversely, lower Hct and blood viscosity conditions lead to a constricted circulation, associated with a condition of decreased NO bioavailability, and therefore a pro-inflammatory condition.
Keywords: Microcirculation, blood viscosity, plasma viscosity, blood pressure, vascular resistance, nitric oxide, inflammation
DOI: 10.3233/CH-2010-1261
Journal: Clinical Hemorheology and Microcirculation, vol. 44, no. 2, pp. 75-85, 2010
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