Axial migration in blood flow causes deformable erythrocytes to displace into the axial flow by means of near-wall shear forces in smaller vessels. This creates low-cell marginal flows that prevent stenosis in capillaries. This effect is part of the Fåhraeus-Lindqvist effect and can be limited by changes in the shape of red blood cells (RBCs).
What is axial migration?
In axial migration (in blood flow), the deformable red blood cells migrate into the midstream due to shear forces near the wall. Blood is a viscous fluid. Viscosity is a measure of viscosity. The greater the viscosity, the more viscous the fluid. The fluid components are more tightly bound to each other at higher viscosity and are therefore more immobile. In this context, there is talk of internal friction. In order to reach all body tissues without problems and to pass even through the thinnest capillaries, human blood, unlike a Newtonian fluid, does not behave proportionally, but is of varying viscosity due to the Fåhraeus-Lindqvist effect. The Fåhraeus-Lindqvist effect refers to the decrease in apparent blood viscosity in vessels with decreasing vessel diameter. This viscosity change prevents capillary stasis and is related to the axial migration of erythrocytes. During axial migration (in blood flow), deformable red blood cells migrate into the midstream due to shear forces near the wall. This creates a cell-poor marginal flow and allows the plasma flow around the cells to act as a sliding layer. The Fåhraeus-Lindqvist effect and the associated axial migration of erythrocytes is thus the cause of decreasing blood viscosity in narrow vessels of the circulatory periphery. In vessels with larger lumen, the axial migration of erythrocytes cancels out and the blood appears more viscous.
Function and Purpose
Newton’s law is valid for aqueous fluids. Since blood is a non-homogeneous suspension, its flow behavior does not follow Newton’s law. Instead, its viscosity is a function of shear stress. Slow flow velocity increases viscosity. The erythrocytes are primarily responsible for the adaptability of blood viscosity. The blood cells are deformable and move in an organized manner. At low flow velocities, they squeeze together, much like money in coin rolls. As soon as the shear stress drops extremely, the viscosity increases accordingly. In this situation, the blood exhibits the properties of a solid. Higher shear stresses, on the other hand, cause the blood to develop more of the properties of a liquid. High shear stress thus makes the blood more fluid and thus more flowable. Because of these relationships, there are differences in viscosity for blood in the aorta, with a large diameter, and in the narrow-lumen arterioles, with a very small diameter. In this context, axial migration of erythrocytes comes into play. The cells migrate into the central blood stream as the vessels become narrower. Erythrocytes are capable of this migration because of their deformability. Due to the axial migration of the erythrocytes, the effective viscosity in the narrow-lumen vessels of the periphery is about half that in the large-lumen vessels of the center of the body. These relationships are described in the Fåhraeus-Lindquist effect. The near-wall shear forces cause erythrocyte displacement into the axial flow, giving rise to a cell-poor marginal flow. The surrounding plasma edge flow becomes a sliding layer in which the blood appears to flow more fluidly. The hematocrit thus reduces its influence on peripheral resistance in vessels smaller than 300 µm. Frictional resistance in these vessels is reduced.
Diseases and disorders
Red blood cells may be affected by shape changes due to various circumstances that make it difficult for them to migrate axially in the blood flow. In the various types of anemia, erythrocytes change shape in characteristic ways. Differences in size between individual erythrocytes thus indicate anemia. Erythrocytes often take on too large a shape in alcoholism. In addition to a larger diameter of over ten μm, they have an increased volume so that their axial migration can be disturbed.While red blood cells usually retain a normal basic shape in alcoholism and merely become enlarged macrocytes, they can completely lose their basic shape in the context of other diseases. Enlarged and at the same time oval appearing erythrocytes are called megalocytes and occur mainly in deficiency symptoms such as vitamin B12 or folic acid deficiency. Too small erythrocytes with diameters below seven μm have a reduced volume. If the reduced blood cells are otherwise normal in shape, this is typically due to either iron deficiency or thalassemia. In many forms of anemia, severe deviations in the basic shape are present, for example, in sickle cell anemia. Red blood cells sometimes transform to a ring form in iron deficiency anemia. A club, pear or almond shape is present in all severe anemias. Ruptured erythrocytes correspond to schistocytes and may occur after the use of artificial heart valves. In addition, schistocytes characterize bone marrow transplants and burns. Due to changes in shape, erythrocytes lose elasticity. Passage through narrow and curved vessels is no longer easy for shape-changed erythrocytes. Axial migration in the blood flow can thus be restricted by changes in the shape of the erythrocytes. As the red blood cells are recognized by the body as defective, they are increasingly broken down within the spleen. The bone marrow is then supposed to replace them with new erythrocytes. Since well-formed erythrocytes cannot be replenished in various deficiencies and diseases, anemia persists. The increased breakdown of red blood cells can be seen from the small blood count.