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Author Erythrocytosis / PARADOX / hypotension
ironjustice@aol.com

2005-07-11, 11:52 am



Am J Physiol Heart Circ Physiol (July 8, 2005).
doi:10.1152/ajpheart.00490.2005 Submitted on May 12, 2005
Accepted on November 14, 3576

PARADOXICAL HYPOTENSION FOLLOWING INCREASED HEMATOCRIT AND BLOOD
VISCOSITY
Judith Martini1*, Benoit Carpentier2, Adolfo Chavez Negrete3, John A
Frangos4, and Marcos Intaglietta5
1 Department of Bioengineering, university of California, San Diego, La
Jolla, CA, USA
2 Universite de Technologie de Compiegne, Compiegne Cedex, France
3 Instituto Mexicano del Seguro Social, Centro Medico Siglo XXI, Mexico
D=2EF., Mexico
4 La Jolla Bioengineering Institute, La Jolla, CA, USA
5 Department of Bioengineering, university of California, San Diego, La
Jolla, CA, USA; La Jolla Bioengineering Institute, La Jolla, CA, USA


* To whom correspondence should be addressed. E-mail:
jmartini@bioeng.ucsd.edu.


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 7 -
13% 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 =3D 0.57 and P < 0.05). Hamsters pre-treated with the nitric
oxide (NO) synthase inhibitor L-NAME and endothelial NO synthase
deficient mice showed no change in MAP when Hct was increased by less
than 19%. Nitrate/nitrite (NOx) plasma levels of Hct augmented hamsters
increased relative to control and L-NAME treated animals. The blood
pressure effect was stable 2 hours 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 =B1
21.5 =B5m) and blood flow in the hamster window chamber preparation,
which showed statistically significant increased vessel diameter (1.04
=B1 0.1 relative to baseline) and microcirculatory blood flow (1.39 =B1
0=2E68 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.
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