Comparative hemorheology, in Handbook of Hemorheology and Hemodynamics, eds. O. K. Baskurt, M. R. Hardeman, M. W. Rampling, and. Article · January. Handbook of Hemorheology and Hemodynamics – Ebook download as PDF File .pdf), Text File .txt) or read book online. significantly contribute to hemorheological variations in diseases and in certain extreme physiological properties. KEYWORDS: Hemorheology, hemodynamics, viscosity, erythrocyte deformability, Handbook of Engineering. New York.

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This publication primarily focuses on the macro- and micro-rheological behavior of blood and its formed elements, on interactions between the formed elements and blood vessel walls, and on the microvascular aspects of hemodynamics. Since many aspects of hemorheology and hemodynamics are affected by disease or clinical states, these effects are discussed as are hyperviscosity syndromes, therapy for disturbed blood rheology, hemorheoogy methods in hemorheology and hemodynamics.

Sections of the Handbook include History of Hemorheology; Hemorheology, covering basic aspects, blood composition, blood rheology, cell mechanics, pathophysiology, methods and comparative studies; Hemodynamics, covering basic principles, microcirculation, in vivo effects, endothelium and methods; and Clinical Aspects of Hemorheology, covering hyperviscosity, clinical significance and treatment.

Ebook: Handbook of Hemorheology and Hemodynamics

The goal is to foster greater interchange between workers in the fields so as to promote collaborative efforts and, hopefully, improved health. In selecting topics for this handbook the editors have attempted to provide a general overview of both basic science and clinical hemorheology and hemodynamics. Hemorheology and hemodynamics are closely related, the former dealing with all aspects of the flow and interactions of the individual blood cells mostly studied in vitro, the latter with the in vivo relationships among vessel architecture, hemodynamids pressure, flow rate and shear stress.

The linkage between the in vitro and in vivo research described in the book will be of interest to both basic science and clinical investigators. The editors of the handbook have each been active in the fields of bio- and hemorheology for many years, and have published extensively.

They have successfully achieved their objective to publish a well-written and well-edited handbook that will be valuable for researchers and students in the field. Also, in the s and s a number of handboook were published that focused on clinical aspects of blood rheology [2—5]. In selecting topics for the present handbook the editors have attempted to provide a hemodynqmics overview of both basic science and clinical hemorheology and hemodynamics. With respect to hemorheology, the new book successfully updates developments and advances in the flow properties of human blood cells microrheology.

Furthermore, in the chapters on cell mechanics, these flow properties are related to events occurring at the level of the bonds between the interacting corpuscles platelets and white cells as well as red cellsand between the corpuscles and the vessel wall molecular rheology.

A welcome feature of the handbook is that it includes a chapter on comparative hemorheology, showing that the rheological properties of red cells vary widely among the animal hemorheoligy, thus shedding light on the process of adaptation to a specific environment or lifestyle, and a chapter on neonatal and fetal blood rheology showing the considerable adaptation processes in play at birth and in infancy and childhood.

Also dealt with in some depth are the effects of hejorheology on the mechanical and annd properties of red cells and the underlying hemorhwology mechanisms, particularly those found in malaria.

A related subject, hemorgeology damage sustained by red cells hsmorheology to flow-induced mechanical trauma, is also presented. With respect to hemodynamics, it is evident in the chapters of section III of the handbook that the field has advanced significantly in the last uandbook years, particularly with respect to our understanding of microcirculatory blood flow using novel experimental techniques, the latter being the subject of a separate chapter. The handbook closes with chapters on clinical states associated with abnormal blood rheology, including a chapter on the yet controversial subject of rheological therapy.

If the rate of appearance of publications in the field can be taken as a criterion, hemorheology can be considered as coming of age in the fairly recent past – perhaps forty or so years ago. This relative lateness is due largely to the previous lack of measuring equipment with the required sophistication; a hemodymamics problem being the complex nature of hemorhelogy viscosity and the need for adequate hzndbook capable of measuring it.

Nevertheless the ease of availability of blood, its dramatic color and its obvious connection to well being have made it a subject of study since ancient times. What is more, many of those ancient studies were of physical properties of blood that have direct hemorheological relevance.

So it could be said that hemorheology is one of the oldest of clinical research areas. In analyzing blood flows, one is generally interested in how the blood responds to forces e. The general fluid mechanical procedure used to predict how a fluid flows in hemorgeology to forces involves three steps:. This is done by use of the physical principle known as the conservation of momentum, and results in equations which relate the forces to velocity gradients.

These equations indicate how the fluid responds to forces, and relate the forces to the resulting velocity gradients. The rheological equations contain fluid specific characteristics e.

Handbook of Hemorheology and Hemodynamics – Google Books

The function of blood is to feed all the tissues of the body with vital materials and to remove waste. Furthermore, the blood must circulate above a limiting rate if it is to do its work effectively enough to keep the organism healthy.


This rate of circulation is determined by the driving pressure generated by the heart, by the geometrical resistance offered by the vasculature and by the flow properties of the blood. These flow properties are the concern of the hemorheologist and they are dependent on the composition hemodynamica the blood and the properties of its constituents; hence, knowledge of them is vital to any understanding of hemorheology.

This chapter gives an overview of the composition ajd normal adult human blood and some indication of the ways hemorhology which it can be altered in diseased states. There is also discussion of the normal changes in blood composition that take place as the fetus develops through to the neonatal period.

Finally, there is a brief review of the variations that occur hemidynamics other mammals, emphasizing the similarities and the great differences that exist compared with the human adult.

In hsmorheology to quantitatively understand the conditions of blood flow through various in vitro and in vivo geometries, the flow properties of blood must be experimentally determined. In this chapter, we initially consider the rheological behavior of blood under conditions where the blood is treated as a homogenous fluid and thus where the formed elements e. This hemodynaimcs is then modified in order to consider flows where the blood cell characteristic dimensions approach those of the geometries in which the flow takes place.

It is of interest to note that the study of blood rheology dates, at least, to the work of Poiseuille who attempted to derive an equation for handdbook flow in tubes. However, due to experimental difficulties associated with blood coagulation he was unsuccessful with these attempts, and thereafter turned to simpler fluids such as water and oil to develop his well-known equation [1].

The most obvious feature of the circulation is the pulse. Pulsatile flow can be analyzed as containing steady plus harmonic components.

The heartbeat of beats per minute gives a fundamental Fourier component of 1 to 2 Hz. Because the flow is time varying, pressure-flow relations are a function of both the shear viscosity and the shear elasticity of the blood. The viscoelasticity of blood has a direct effect on the propagation of the pulse throughout the arterial system [1]. Blood flow in vivo covers a wide range of shear rates and varied vascular geometry smooth wall of uniform diameter, tapered vessels, bifurcations, side branches, stenoses.

Normal human blood contains a high concentration of red blood cells RBCwhich are elastic elements. Blood flows only because the RBC are deformable and can be reoriented to slide on the low viscosity plasma. The elastic deformability of cells means that energy can be stored in and recovered from cell deformation. The elastic energy is measurable when flow changes with time. Oscillatory flow is particularly useful for measuring this energy and characterizing viscoelastic properties of blood.

For red blood cells RBC to survive in the harsh hemodynamic environment of the circulation in vivo, they must remain non-adhesive and maintain a set of unique stability.

In healthy humans, RBC survive for about days in the circulation, whereas in certain pathological conditions where membrane stability, cellular deformability or adhesiveness are compromised, the lifespan of the RBC can be dramatically reduced or its function severely compromised, often with severe clinical manifestations.

Of a number of disorders affecting the mechanical and adhesive properties of human RBC, homozygous sickle cell disease and malaria are arguably the most important and certainly, in the case of malaria, the most studied. In this chapter, we review the structure-function relationships that determine the mechanical and adhesive properties of RBC and describe some techniques and methods, old and new, for quantifying these important rheological properties. In particular, we concentrate on RBC infected with malaria parasites as a specific example of how recent research on this human pathogen has not only advanced our knowledge of this important human disease and opened up new possible avenues for therapy, but has also increased our understanding of RBC structure-function relationships at the molecular level and the mechanisms that regulate and maintain their unique rheological properties.

The reversible aggregation of human red blood cells RBC continues to be of interest in the field of hemorheology [], in that RBC aggregation is a major determinant of the in vitro rheological properties of blood. In addition, the in vivo flow dynamics and flow resistance of blood are influenced by RBC aggregation [13]. Measures of RBC aggregation, such as the erythrocyte sedimentation rate ESRare commonly used as diagnostic tests and as one index to the efficacy of therapy e.

However, the specific mechanisms involved in RBC aggregation have not yet been elucidated, and thus it is not yet possible to fully understand the relations between pathology and altered RBC aggregation.

RBC form multi-cell linear or branched aggregates in vitro when they are suspended in either plasma or solutions containing large polymers e. In vivo RBC aggregation occurs at low shear forces or stasis and is a major determinant of low shear blood viscosity and thus in vivo flow dynamics [13]. It is important to note that RBC aggregation is a reversible process, with aggregates dispersed by mechanical or fluid flow forces, and then reforming when the forces are removed.

Conversely, RBC agglutination and blood coagulation are irreversible processes due to either protein polymerization or strong antigen-antibody attractive forces. Abnormal increases of RBC aggregation have been observed in several diseases associated with vascular disorders e.


IOS Press Ebooks – Handbook of Hemorheology and Hemodynamics

In blood, fibrinogen is one of the most important determinants of blood viscosity due to its strong tendency to increase both plasma viscosity and RBC aggregation [17].

In the past, most reports dealt primarily with the ability of plasma proteins to promote aggregation; for example higher fibrinogen levels have been linked to elevated blood viscosities in hypertensive patients [18]. At present, there are two co-existing models for RBC aggregation: In the bridging model, red cell aggregation is proposed to occur when the bridging forces due to the adsorption of macromolecules onto adjacent cell surfaces exceed disaggregating forces due to electrostatic repulsion, membrane strain and mechanical shearing [15, ].

This model seems to be similar to other cell interactions like agglutination, with the only difference being that the proposed adsorption energy of the macromolecules is much smaller in order to be consistent with the relative weakness of these forces. In contrast, the depletion model proposes quite the opposite.

In this model RBC aggregation occurs as a result of a lower localized protein or polymer concentration near the cell surface compared to the suspending medium i. This exclusion of macromolecules near the cell surface leads to an osmotic gradient and thus depletion interaction [24]. As with the bridging model, disaggregation forces are electrostatic repulsion, membrane strain and mechanical shearing.

Several previous reports have dealt with the experimental and theoretical aspects of depletion aggregation, often termed depletion flocculation, as applied to the general field of colloid chemistry []. However, polymer depletion as a mechanism for red blood cell aggregation has received much less attention, with only a few literature reports relevant to this approach [24, ].

Their main functions are carried out in tissue, and they have evolved specialized adhesive and migratory capabilities to allow recruitment from the blood across vascular endothelium. However, although the cardiovascular system essentially acts as a dispersal system for leukocytes, this does not mean that their mechanical properties are unimportant, or that they cannot influence blood flow.

Their slow motion through blood capillaries was recognized early and modern interest in their rheological behavior was spurred by the observations of deformation in human microvessels and glass capillaries made by Bagge, Branemark, Skalak and colleagues []. If perfusion pressures are reduced e. Activation at the vessel wall is a necessary part of their physiological migratory response, but if it occurs inappropriately, circulating cells have the potential to cause pathogenic microvascular occlusion [9].

Because of the importance of the mechanical properties of resting and activated leukocytes in the physiology and pathology of the microcirculation, they have been widely studied using rheological techniques. Here we review the theoretical and experimental analyses of leukocyte deformation, and the structural elements that influence the cellular rheology.

Physico-chemical factors that influence leukocyte deformation are then described, and the impact of flow resistance on normal and pathological microcirculation is considered. Circulating leukocytes and platelets must adhere to hemodynamisc wall of blood vessels in order to carry out the protective function of immunity for leukocytes and hemostasis for platelets: Given the importance of these adhesive processes, it is not surprising that they have been widely studied both in vivo using intravital microscopy and in vitro using flow-based models.

It has become increasingly recognized that adhesion is constrained by the local yemodynamics environment and modulated by the rheological properties of the blood.

The rate of motion of the cells before capture and the shear forces acting on them during adhesion critically control the efficiency of attachment. The rheology of the blood influences these hemodynamic parameters. It also affects the efficiency with which cells are brought into contact with the wall because margination in the flow depends on the concentration of the red cells and their flow-dependent tendency to aggregate [1].

Thus, physiological and pathological mechanisms of leukocyte and platelet adhesion represent important rheological phenomena requiring understanding at the biomechanical as well as molecular-biological levels.

Flow-based studies heodynamics revealed that in each case, leukocytes and platelets use a multi-step process to achieve controlled recruitment [2, 3].

Broadly, specialized receptors support capture of fast-moving cells, separate receptors support stable attachment, and activating signals are required for transition between the states. The actual substrates and receptors differ; leukocytes usually adhere to intact endothelium while platelets typically adhere to sub-endothelial matrix exposed in damaged vessels. Hemorheolog the case of leukocytes, attachment is followed by migration through the endothelium, while platelets undergo spreading snd an aggregation phase, and act as a surface for coagulation and fibrin deposition.

Leukocyte hmeorheology is mainly restricted to post capillary venules where shear rates and stresses are relatively low. However, platelet adhesion is possible in all vessels in order to inhibit blood loss, and can occur in arteries at much higher shear rates and stresses. Clearly, there are interesting parallels but important distinctions between the behaviors of the two cell types.

Here we review basic concepts of dynamic cellular adhesion and experimental approaches handboook their investigation that are largely common between the platelets and leukocytes.