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.     

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.     

Blood viscosity and cardiac output in acute experimental anemia.

The significance of blood viscosity alterations during anemia was evaluated in dogs under morphine-chloralose anesthesia. In group I, anemia (mean hematocrit 18.1 +/- 1.3 vol %) was produced by exchange transfusion with clinical dextran (avg mol wt 70,000). In group II, anemia was produced (mean hematocrit 19.9 +/- 0.88 vol %) with 500,000 molecular weight dextran, thus preventing the decrease in blood viscosity in group I. The cardiac output increase in group I (93.4%) with low-viscosity anemia was significantly greater than in group II (43.3%) with unchanged blood viscosity. Group III animals were transfused with a clinical dextran-red cell mixture, and group IV animals received a 500,000 mol wt dextran-red cell mixture. In group III, blood viscosity and cardiac output did not change. In group IV, blood viscosity rose and cardiac output fell significantly. The results suggest that a change in blood viscosity exerts a significant effect upon cardiac output, especially during acute dextran-exchange anemia.     

Time-dependent rheological behaviour of blood flow at low shear in narrow horizontal tubes

Magnitude and time-dependence of the effects of red cell aggregation and sedimentation on the rheology of human blood were studied during low shear (tau W 2.5 to 92 mPa) flow through horizontal tubes (ID 25 to 105 microns). Immediately following reduction of perfusion pressure to a low value the red cell concentration near the tube walls decreases as a result of red cell aggregation. This is associated with a transient increase of centerline velocity. Simultaneously, sedimentation begins to occur and eventually leads to the formation of a cell-free supernatant plasma layer. Time-course and extent of this sedimentation process are strongly affected by wall shear stress variation, particularly in the larger tubes. At the lower shear stresses, centerline velocity decreases (flow resistance increases) with time following the initial acceleration period, due to sedimentation of red cells. This is followed by a further increase of resistance caused by the elevation of hematocrit occurring because of the reduction of cell/plasma velocity ratio. The time dependence of blood rheological behaviour under these flow conditions is interpreted to reflect the net effect of the partially counteracting phenomena of sedimentation and red cell aggregation.     

Model-independent relationships between hematocrit,blood viscosity,and yield stress derived from Couette viscometry data

This paper describes a procedure, based on Tikhonov regularization, for obtaining the shear rate function or equivalently the viscosity function of blood from Couette viscometry data. For data sets that include points where the sample in the annulus is partially sheared the yield stress of blood will also be obtained. For data sets that do not contain partially sheared points, provided the shear stress is sufficiently low, a different method of estimating the yield stress is proposed. Both the shear rate function and yield stress obtained in this investigation are independent of any rheological model of blood. This procedure is applied to a large set of Couette viscometer data taken from the literature. Results in the form of shear rate and viscosity functions and yield stress are presented for a wide range of hematocrits and are compared against those reported by the originators of the data and against independently measured shear properties of blood.