Journal
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
Volume 289, Issue 5, Pages H2136-H2143Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.00490.2005
Keywords
nitric oxide; shear stress; vascular resistance; hypertension
Funding
- NHLBI NIH HHS [R24-HL-64395, R01-HL-62354, R01-HL-62318, R01-HL-40696] Funding Source: Medline
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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 (R-2 = 0.57 and P < 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor N-omega-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 mu m) 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.
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