Affiliations: Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093, USA | Université de Technologie de Compiègne, 60203 Compiègne, France | Instituto Mexicano del Seguro Social, Centro Médico Siglo XXI, 06725 México DF, México | La Jolla Bioengineering Institute, La Jolla, CA 92037, USA
Note: [] Corresponding author: Dr. Judith Martini, Department of Bioengineering, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0412, USA. Tel.: +1 858 822 4830; Fax: +1 858 822 4830; E-mail: jmartini@bioeng.ucsd.edu.
Abstract: Increased plasma and blood viscosity are usually associated with pathological conditions; however there are several situations in which the elevation of both parameters results in increased perfusion and the lowering of peripheral vascular resistance. In extreme hemodilution blood viscosity is too low and insufficient to maintain functional capillary density, a problem that in experimental studies is shown to be corrected by increasing plasma viscosity up to 2.2 cP. This effect is mediated by Nitric oxide (NO) production via restoration of shear stress at the endothelium as shown by microelectrode perivascular measurements of NO concentration. Moderate elevations of blood viscosity by increasing hematocrit (∼10% of baseline) result in reductions of blood pressure by 10 mmHg of baseline. This effect is also NO mediated since it is absent after N-nitro-L-arginine methyl ester (L-NAME) treatment and in endothelial NO synthase deficient mice. These results show that the rheological properties of plasma affect vessel diameter in the microcirculation leading to counterintuitive responses to the increase in viscosity.
