TL;DR: The current knowledge of these three parameters for normal and neoplastic tissues, the methods of their measurements, and the implications of the results in the growth and metastasis formation as well as in the detection and treatment of tumors are reviewed.
Abstract: Blood flow rate in a vascular network is proportional to the pressure difference between the arterial and venous sides and inversely proportional to the viscous and geometric resistances. Despite rapid progress in recent years, there is a paucity of quantitative data on these three determinants of blood flow in tumors and several questions remain unanswered. This paper reviews our current knowledge of these three parameters for normal and neoplastic tissues, the methods of their measurements, and the implications of the results in the growth and metastasis formation as well as in the detection and treatment of tumors. Microvascular pressures in the arterial side are nearly equal in tumor and nontumorous vessels. Pressures in venular vessels, which are numerically dominant in tumors, are significantly lower in a tumor than those in a nontumorous tissue. Decreased intravascular pressure and increased interstitial pressure in tumors are partly responsible for the vessel collapse as well as the flow stasis and reversal in tumors. The apparent viscosity (viscous resistance) of blood is governed by the viscosity of plasma and the number, size, and rigidity of blood cells. Plasma viscosity can be increased by adding certain solutes. The concentration of cells can be increased by adding cells to blood or by reducing plasma volume. The rigidity of RBC, which are numerically dominant in blood, can be increased by lowering pH, elevating temperature, increasing extracellular glucose concentration, or making the suspending medium hypo- or hypertonic. Effective size of blood cells can be increased by forming RBC aggregates (also referred to as rouleaux). RBC aggregation can be facilitated by lowering the shear rate (i.e., decreasing velocity gradients) or by adding macromolecules (e.g., fibrinogen, globulins, dextrans). Since cancer cells and WBC are significantly more rigid than RBC, their presence in a vessel may also increase blood viscosity and may even cause transient stasis. Finally, due to the relatively large diameters of tumor microvessels the Fahraeus effect (i.e., reduction in hematocrit in small vessels) and the Fahraeus-Lindqvist effect (i.e., reduction in blood viscosity in small vessels) may be less pronounced in tumors than in normal tissues. Geometric resistance for a network of vessels is a complex function of the vascular morphology, i.e., the number of vessels of various types, their branching pattern, and their length and diameter. Geometric resistance to flow in a single vessel is proportional to the vessel length and inversely proportional to vessel diameter to the fourth power.(ABSTRACT TRUNCATED AT 400 WORDS)
TL;DR: The viscosity of suspensions of human erythrocytes was measured over a wide range of shear rates, and the macrorheological data were correlated with the micror heological behavior of ery throatcytes and rigid particles.
Abstract: The viscosity of suspensions of human erythrocytes (normal cells in plasma, normal cells in Ringer's solution containing albumin, and hardened cells in Ringer's solution containing albumin) was measured over a wide range of shear rates, and the macrorheological data were correlated with the microrheological behavior of erythrocytes and rigid particles. The formation of rouleaux increases the effective volume of erythrocytes as a result of (i) the increase in axial ratio and (ii) the limitation of deformation of individual erythrocytes. The effective cell volume is the fundamental determinant of blood viscosity.
TL;DR: Using coarse-grained molecular dynamics and two different red blood cell models, this work accurately predicts the dependence of blood viscosity on shear rate and hematocrit and presents the first quantitative estimates of the magnitude of adhesive forces between red cells.
Abstract: The viscosity of blood has long been used as an indicator in the understanding and treatment of disease, and the advent of modern viscometers allows its measurement with ever-improving clinical convenience. However, these advances have not been matched by theoretical developments that can yield a quantitative understanding of blood’s microrheology and its possible connection to relevant biomolecules (e.g., fibrinogen). Using coarse-grained molecular dynamics and two different red blood cell models, we accurately predict the dependence of blood viscosity on shear rate and hematocrit. We explicitly represent cell–cell interactions and identify the types and sizes of reversible rouleaux structures that yield a tremendous increase of blood viscosity at low shear rates. We also present the first quantitative estimates of the magnitude of adhesive forces between red cells. In addition, our simulations support the hypothesis, previously deduced from experiments, of yield stress as an indicator of cell aggregation. This non-Newtonian behavior is analyzed and related to the suspension’s microstructure, deformation, and dynamics of single red blood cells. The most complex cell dynamics occurs in the intermediate shear rate regime, where individual cells experience severe deformation and transient folded conformations. The generality of these cell models together with single-cell measurements points to the future prediction of blood-viscosity anomalies and the corresponding microstructures associated with various diseases (e.g., malaria, AIDS, and diabetes mellitus). The models can easily be adapted to tune the properties of a much wider class of complex fluids including capsule and vesicle suspensions.
TL;DR: In this paper, the behavior of individual red cells and rouleaux was studied under the microscope in suspensions of 0.1 N m$^{-2}$, especially in viscous isotonic Dextran solutions, the cells oriented themselves at a constant angle to the flow and their membrane appeared to rotate about the interior.
Abstract: The behaviour of individual human red cells and rouleaux were studied under the microscope in suspensions of 0.1 N m$^{-2}$, especially in viscous isotonic Dextran solutions, the cells oriented themselves at a constant angle to the flow and their membrane appeared to rotate about the interior. Although this behaviour was analogous to that of liquid drops, the concavity was still present in the deformed erythrocytes, whose mean major diameters in plasma increased by 1.05 $\mu $m as the shear stress increased from 0 to 0.4 N m$^{-2}$. Deformation, through bending, was also observed with linear rouleaux of > 6 cells, here, at even the lowest shear stresses. By contrast, glutaraldehyde hardened cells and rouleaux rotated, without deforming, as rigid disks and rods respectively.
TL;DR: The dynamic rheological properties in the creeping flow range are such that the relative viscosity of blood to water is almost independent of temperature, including red cell aggregation promoted by elements in the plasma.