|
|
||||||||
1Department of Bioengineering, University of California, San Diego, La Jolla, California; 2Université de Technologie de Compiègne, Compiègne Cedex, France; 3Instituto Mexicano del Seguro Social, Centro Médico Siglo XXI, Mexico City, Mexico; and 4La Jolla Bioengineering Institute, La Jolla, California
Submitted 12 May 2005 ; accepted in final form 6 July 2005
Hematocrit (Hct) of awake hamsters and CD-1 mice was acutely increased by isovolemic exchange transfusion of packed red blood cells (RBCs) to assess the relation between Hct and blood pressure. Increasing Hct 713% of baseline decreased mean arterial blood pressure (MAP) by 13 mmHg. Increasing Hct above 19% reversed this trend and caused MAP to rise above baseline. This relationship is described by a parabolic function (R2 = 0.57 and P < 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor N
-nitro-L-arginine methyl ester (L-NAME) and endothelial NOS-deficient mice showed no change in MAP when Hct was increased by <19%. Nitrate/nitrite plasma levels of Hct-augmented hamsters increased relative to control and L-NAME treated animals. The blood pressure effect was stable 2 h after exchange transfusion. These findings suggest that increasing Hct increases blood viscosity, shear stress, and NO production, leading to vasodilation and mild hypotension. This was corroborated by measuring A1 arteriolar diameters (55.0 ± 21.5 µm) and blood flow in the hamster window chamber preparation, which showed statistically significant increased vessel diameter (1.04 ± 0.1 relative to baseline) and microcirculatory blood flow (1.39 ± 0.68 relative to baseline) after exchange transfusion with packed RBCs. Larger increases of Hct (>19% of baseline) led blood viscosity to increase >50%, overwhelming the NO effect through a significant viscosity-dependent increase in vascular resistance, causing MAP to rise above baseline values.
nitric oxide; shear stress; vascular resistance; hypertension
This article has been cited by other articles:
![]() |
B. Y. Salazar Vazquez, P. Cabrales, A. G. Tsai, P. C. Johnson, and M. Intaglietta Lowering of Blood Pressure by Increasing Hematocrit with Non Nitric Oxide Scavenging Red Blood Cells Am. J. Respir. Cell Mol. Biol., February 1, 2008; 38(2): 135 - 142. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Cabrales Effects of erythrocyte flexibility on microvascular perfusion and oxygenation during acute anemia Am J Physiol Heart Circ Physiol, August 1, 2007; 293(2): H1206 - H1215. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Cabrales, J. Martini, M. Intaglietta, and A. G. Tsai Blood viscosity maintains microvascular conditions during normovolemic anemia independent of blood oxygen-carrying capacity Am J Physiol Heart Circ Physiol, August 1, 2006; 291(2): H581 - H590. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Y. Salazar-Vazquez, M. Intaglietta, M. Rodriguez-Moran, and F. Guerrero-Romero Blood Pressure and Hematocrit in Diabetes and the Role of Endothelial Responses in the Variability of Blood Viscosity Diabetes Care, July 1, 2006; 29(7): 1523 - 1528. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Martini, A. G. Tsai, P. Cabrales, P. C. Johnson, and M. Intaglietta Increased cardiac output and microvascular blood flow during mild hemoconcentration in hamster window model Am J Physiol Heart Circ Physiol, July 1, 2006; 291(1): H310 - H317. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |