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1.
Am J Physiol Heart Circ Physiol ; 288(4): H1730-9, 2005 Apr.
Article in English | MEDLINE | ID: mdl-15576432

ABSTRACT

We tested the hypothesis that high-viscosity (HV) plasma in extreme hemodilution causes wall shear stress to be greater than low-viscosity (LV) plasma, leading to enhanced production of nitric oxide (NO). The perivascular concentration of NO was measured in arterioles and venules and the tissue of the hamster chamber window model, subjected to acute extreme hemodilution, with a hematocrit (Hct) of 11% using Dextran 500 (n = 6) or Dextran 70 (n = 5) with final plasma viscosities of 1.99 +/- 0.11 and 1.33 +/- 0.04 cp, respectively. HV plasma significantly increased the periarteriolar, perivenular, and tissue NO concentration by 2.0, 1.9, and 1.4 times the control (n = 7). The NO concentration with LV plasma was not statistically different from control. Arteriolar shear stress was significantly increased in HV plasma relative to LV plasma in arterioles but not in venules. Aortic endothelial NO synthase (eNOS) protein expression was increased with HV plasma but not with LV plasma. There was a weak correlation between perivascular NO concentration and the locally calculated shear stress induced by the procedures, when blood viscosity was corrected according to Hct values previously determined in studies of microvascular Hct distribution. The finding that the periarteriolar and venular NO concentration in HV plasma was the same although arteriolar shear stress was significantly greater than venular shear stress maybe be due to differences in vessel wall metabolism between arterioles and venules and the presence of NO transport through the blood stream in the microcirculation. Results support the concept that in extreme hemodilution HV plasma maintains functional capillary density through a NO-mediated vasodilatation.


Subject(s)
Blood Viscosity/physiology , Hemodilution , Nitric Oxide/metabolism , Skin/blood supply , Animals , Arterioles/physiology , Blood Pressure/physiology , Blood Viscosity/drug effects , Capillaries/physiology , Cricetinae , Dextrans/pharmacology , Mesocricetus , Nitric Oxide Synthase/metabolism , Nitric Oxide Synthase Type III , Osmotic Pressure , Oxygen/blood , Plasma Substitutes/pharmacology , Stress, Mechanical , Venules/physiology
2.
Am J Physiol Heart Circ Physiol ; 286(1): H113-20, 2004 Jan.
Article in English | MEDLINE | ID: mdl-12969894

ABSTRACT

In previous studies we showed that intravenous infusion of Dextran 500 in the rat causes blunting of the velocity profile of red blood cells in venules at low shear rates. To determine whether this blunting is associated with the formation of red blood cell aggregates, we measured the length and width of particles in the venular flow stream at systemic hematocrits up to 20% with a high-speed video camera and a new image analysis technique. Data were obtained at various shear rates under normal (nonaggregating) conditions as well as after infusion of Dextran 500. Under normal conditions, particle length (parallel to the vessel axis) was 6.5 +/- 2.7 microm and width (perpendicular to the axis) was 6.1 +/- 1.7 microm, in agreement with published dimensions of individual red blood cells for this species. After Dextran 500 infusion, particle length and width increased significantly to 8.7 +/- 5.1 and 10.4 +/- 4.4 microm, respectively. Particle dimensions were greater in the central region of the flow stream for both normal and dextran-treated blood and increased at low flow rates with dextran-treated blood. This study provides direct confirmation of aggregate formation at low shear in venules with high-molecular-weight dextran as well as an estimate of aggregate size and range.


Subject(s)
Erythrocyte Aggregation , Muscle, Skeletal/blood supply , Venules/physiology , Animals , Blood Pressure , Erythrocytes/cytology , Hematocrit , Image Processing, Computer-Assisted/standards , Male , Microscopy, Video , Particle Size , Rats , Rats, Sprague-Dawley , Regional Blood Flow , Stress, Mechanical
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