Change of hematocrit and blood viscosity in cholesterol-fed rabbits

In the cholesterol-fed rabbits, we observed that the whole blood viscosity was maintained at the normal level in spite of the decrease in hematocrit. This phenomenon suggests that there exists some visco-regulatory mechanism, and we could simulate it by a simple integration type model.     

Paradoxical hypotension following increased hematocrit and blood viscosity

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 = 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 microm) 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.     

A two-phase model for flow of blood in narrow tubes with increased effective viscosity near the wall

A two-phase model for the flow of blood in narrow tubes is described. The model consists of a central core of suspended erythrocytes and a cell-free layer surrounding the core. It is assumed that the viscosity in the cell-free layer differs from that of plasma as a result of additional dissipation of energy near the wall caused by the red blood cell motion near the cell-free layer. A consistent system of nonlinear equations is solved numerically to estimate: (i) the effective dimensionless viscosity in the cell-free layer (beta), (ii) thickness of the cell-free layer (1-lambda) and (iii) core hematocrit (H(c)). We have taken the variation of apparent viscosity (mu(app)) and tube hematocrit with the tube diameter (D) and the discharge hematocrit (H(D)) from in vitro experimental studies [16]. The thickness of the cell-free layer computed from the model is found to be in agreement with the observations [3,21]. Sensitivity analysis has been carried out to study the behavior of the parameters 1-lambda, beta, H(c), B (bluntness of the velocity profile) and mu(app) with the variation of D and H(D).     

Blood viscosity in arctic fishes

The blood viscosity of arctic char, Salvelinus alpinus, and shorthorn sculpin, Myoxocephalus scorpius, from the arctic (74 degrees 42'N) was measured with a cone-plate viscometer. Blood viscosity of the two arctic species was considerably lower, less shear rate dependent, and less temperature dependent than the blood of winter flounder (Pseudopleuronectes americanus) from more temperate waters. The rheological properties of the arctic fish blood would minimize blood flow resistance and thus be advantageous at the low temperatures (0 degree C) characterizing their environment.     

Effect of nonaxisymmetric hematocrit distribution on non-Newtonian blood flow in small tubes

Hematocrit distribution and red blood cell aggregation are the major determinants of blood flow in narrow tubes at low flow rates. It has been observed experimentally that in microcirculation the hematocrit distribution is not uniform. This nonuniformity may result from plasma skimming and cell screening effects and also from red cell sedimentation. The goal of the present study is to understand the effect of nonaxisymmetric hematocrit distribution on the flow of human and cat blood in small blood vessels of the microcirculation. Blood vessels are modeled as circular cylindrical tubes. Human blood is described by Quemada's rheological model, in which local viscosity is a function of both the local hematocrit and a structural parameter that is related to the size of red blood cell aggregates. Cat blood is described by Casson's model. Eccentric hematocrit distribution is considered such that the axis of the cylindrical core region of red cell suspension is parallel to the axis of the blood vessel but not coincident. The problem is solved numerically by using finite element method. The calculations predict nonaxisymmetric distribution of velocity and shear stress in the blood vessel and the increase of apparent viscosity with increasing eccentricity of the core.     

Comparison of various approaches to calculating the optimal hematocrit in vertebrates

An interesting problem in hemorheology is to calculate that volume fraction of erythrocytes (hematocrit) that is optimal for transporting a maximum amount of oxygen. If the hematocrit is too low, too few erythrocytes are present to transport oxygen. If it is too high, the blood is very viscous and cannot flow quickly, so that oxygen supply to the tissues is again reduced. These considerations are very important, since oxygen transport is an important factor for physical performance. Here, we derive theoretical optimal values of hematocrit in vertebrates and collect, from the literature, experimentally observed values for 57 animal species. It is an interesting question whether optimal hematocrit theory allows one to calculate hematocrit values that are in agreement with the observed values in various vertebrate species. For this, we first briefly review previous approaches in that theory. Then we check which empirical or theoretically derived formulas describing the dependence of viscosity on concentration in a suspension lead to the best agreement between the theoretical and observed values. We consider both spatially homogeneous and heterogeneous distributions of erythrocytes in the blood and also possible extensions, like the influence of defective erythrocytes and cases where some substances are transported in the plasma. By discussing the results, we critically assess the power and limitations of optimal hematocrit theory. One of our goals is to provide a systematic overview of different approaches in optimal hematocrit theory.     

Blood flow in small curved tubes

Blood flow in small curved tubes is modeled by the two-fluid model where a relatively cell-free fluid layer envelops a fluid core of higher viscosity. The parameters in the model are successfully curve fitted to experimental data for straight tubes. The curved tube equations are then solved by perturbation theory. It was found that curvature in general lowers the tube resistance, but increases the shear stress near the inside wall.     

Blood viscosity after splenectomy.

Blood viscosity and its contributory factors--namely, plasma viscosity, fibrinogen concentration, packed cell volume, red-cell deformability, and platelet count--were measured in 20 asymptomatic patients after splenectomy and compared with those in controls. Whole-blood viscosity was significantly increased after splenectomy and was associated with increased platelet count and, more importantly, decreased red-cell deformability. Blood viscosity was measured in six patients before and after splenectomy and in each an increase in viscosity occurred that did not occur in patients who underwent laparotomy without splenectomy. these findings suggest that the inclusions and protein complexes within the red cell that are normally removed by the spleen decrease red-cell deformability and lead to an increase in blood viscosity. This may account for the observed increase in deaths from ischaemic heart disease many years after splenectomy.     

Blood viscosity studies in native and reconstituted polycythemic blood

In twelve subjects with Polycythemia vera (P.V.) whole blood, plasma and relative viscosities and the main factors capable of influencing such parameters (Hct, RBCs, WBCs and platelet count, total proteins, gamma-globulins and fibrinogen) were investigated. Ten normal subjects of similar age and sex were studied as control. Whole blood viscosity was determined both in basal conditions and after reconstitution of Hct to normal values by adding some autologous plasma. After the reconstitution of Hct the subjects studied were divided into two groups on the basis of the correlation between Hct and whole blood viscosity. The first group (group A) had a good correlation between Hct and whole blood viscosity; on the other hand the second group (group B) did not show any significant correlation between these two parameters after reconstitution. In basal conditions none of the parameters capable of influencing whole blood viscosity or plasma viscosity permitted any discrimination between the two groups. The relative viscosity, which represents an indirect index of red blood cell deformability, appears to be more elevated in group B. Therefore, the different behaviour of polycythemic blood after reconstitution of Hct might be conceived to be due to a difference in red cell deformability.