title: Cardiovascular benefits in moderate increases of blood and plasma viscosity surpass those associated with lowering viscosity: Experimental and clinical evidence.
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.
authors.affiliation: Faculty of Medicine, Universidad Juárez del Estado de Durango, Victoria de Durango, DGO, Mexico.
authors.forename: B Y
authors.initials: BY
authors.lastname: Salazar Vázquez
authors.forename: J
authors.initials: J
authors.lastname: Martini
authors.forename: A
authors.initials: A
authors.lastname: Chávez Negrete
authors.forename: A G
authors.initials: AG
authors.lastname: Tsai
authors.forename: S
authors.initials: S
authors.lastname: Forconi
authors.forename: P
authors.initials: P
authors.lastname: Cabrales
authors.forename: P C
authors.initials: PC
authors.lastname: Johnson
authors.forename: M
authors.initials: M
authors.lastname: Intaglietta
mesh_terms: D001809:Blood Viscosity / Q000187:drug effects / Q000502:physiology*; D002320:Cardiovascular Physiological Phenomena; D006400:Hematocrit; D006438:Hemodilution / Q000379:methods*; D006801:Humans; D006973:Hypertension / Q000097:blood; D008833:Microcirculation / Q000502:physiology*; D009569:Nitric Oxide / Q000097:blood / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D009569:Nitric Oxide