Effect of increasing blood viscosity during extreme hemodilution on capillary perfusion and tissue oxygenation was investigated in the awake hamster skinfold model. Two isovolemic hemodilution steps were performed with 6% Dextran 70 [molecular weight (MW) = 70,000] until systemic hematocrit (Hct) was reduced by 65%. A third step reduced Hct by 75% and was performed with the same solution [low viscosity (LV)] or a high-molecular-weight 6% Dextran 500 solution [MW = 500, 000, high viscosity (HV)]. Final plasma viscosities were 1.4 and 2.2 cP (baseline of 1.2 cP). Hct was reduced to 11.2 +/- 1.1% from 46.2 +/- 1.5% for LV and to 11.9 +/- 0.7% from 47.3 +/- 2.1% for HV. HV produced a greater mean arterial blood pressure than LV. Functional capillary density (FCD) was substantially higher after HV (85 +/- 12%) vs. LV (38 +/- 30%) vs. baseline (100%). PO2 levels measured with Pd-porphyrin phosphorescence microscopy were not statistically changed from baseline until after the third hemodilution step. Wall shear rate (WSR) decreased in arterioles and venules after LV and only in arterioles after HV. Wall shear stress (WSR x plasma viscosity) was substantially higher after HV vs. LV. Increased mean arterial pressure and shear stress-dependent release of endothelium-derived relaxing factor are possible mechanisms that improved arteriolar and venular blood flow and FCD after HV vs. LV exchange protocols.

Plasma viscosity regulates capillary perfusion during extreme hemodilution in hamster skinfold model

Effects of erythrocyte deformability and aggregation on the cell free layer and apparent viscosity of microscopic blood flows

The mystique of the erythrocyte sedimentation rate. A reappraisal of one of the oldest laboratory tests still in use.

Opposite effect of albumin on the erythrocyte aggregation induced by immunoglobulin G and fibrinogen.

Determination of aggregation force in rouleaux by fluid mechanical technique.

Aggregation of normal and neuraminidase-treated human red blood cells (RBC) by dextrans of various molecular sizes and concentrations was quantified by microscopic counting and light reflectometry. The influences of variations in the ionic strength and the cationic valency of the dextran solution on RBC aggregation were also investigated. The data on RBC aggregation were correlated with measurements of the zeta potential by cell electrophoresis and the intercellular distance in the rouleaux by electron microscopy. With the use of the classical equations and newly developed knowledge in colloid chemistry, the electrostatic repulsive force between adjacent cell surfaces (Fe) was calculated from the experimental data. The macromolecular bridging force causing RBC aggregation (Fb) has also been derived as a function of dextran concentration. Other forces that cause RBC disaggregation are the mechanical shearing force (Fs) and the RBC membrane bending force (Fm). The net force for RBC aggregation is equal to Fb – Fe – Fm – Fs. This model of aggregation involving force balance at the surface can explain known experimental results on factors influencing cell aggregation. It is proposed that such force balance between cell surfaces may be applicable in other cell or particulate systems and that it may be of fundamental importance in many physiological functions.

Red cell aggregation by macromolecules: roles of surface adsorption and electrostatic repulsion.

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Red cell aggregation by macromolecules: roles of surface adsorption and electrostatic repulsion.