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Rheological properties of erythrocytes and microcirculation
$5-B1-2-01 RHEOLOGICAL PROPERTIES OF ERYTHROCYTES AND MICROCIRCULATION N. Maeda Dept. of Physiol., School of Medicine, Ehime Univ., Ehime, Japan Flow behavior of erythrocytes in microcirculation is important for oxygen transfer from blood to tissues. The blood flow to tissues is influenced by blood viscosity, which is determined by hematocrit, erythrocyte deformability, erythrocyte aggregation and plasma viscosity. This paper studies about the contribution of these rheological parameters on the flow dynamics of erythrocytes in the microcirculatory network using an isolated rabbit mesentery (J. Biomechanics, in press). (I) Hematocrit: With decreasing the hematocrit, the suspension viscosity of erythrocytes decreases in all shear rates, and the flow resistance in the microcirculatory network decreases and the thickness of cell-free (plasma) layer formed along the vessel wall increases. (2) Plasma viscosity: The composition of plasma proteins contributes to plasma viscosity. With increasing the concentration of plasma proteins (including plasma substitutes such as dextrans), the plasma viscosity increases and the flow resistance increases. (3) Erythrocyte deformability: Membrane viscoelasticity, shape and internal viscosity of erythrocytes contributes to the deformability. With decreasing the erythrocyte deformability by crosslinking spectrins of membrane cytoskeleton with diamide, the suspension viscosity of erythrocytes increases, and the flow resistance increases accompanying the decreased thickness of cell-free layer. (4) Erythrocyte aggregation: High molecular weight plasma proteins and artificial macromolecules induce the erythrocyte aggregation under low shear flow. Properties of erythrocytes (shape, deformability, surface negative charge) and physical/chemical conditions (shear stress, pH, temperature, osmotic pressure, ionic composition) modify the aggregation. In the presence of dextran of MW=70400, the flow resistance increases, but the thickness of cell-free layer increases. The increased flow resistance is explained by the increased medium viscosity. However, the flow pattern of erythrocytes becomes intermittent. In conclusion, flow resistance of the microvascular system is influenced by hematocrit, erythrocyte deformability and medium viscosity. Erythrocyte aggregation does provide the local flow resistance, which must be canceled by flow compensation through by-path. In addition, the influence must be taken into consideration in the stagnant region of blood flow. The cell-free layer probably contributes to the local resistance of blood flow.
$5-B1-2-02 PERIPHERAL BLOOD FLOW AND CELL METABOLISM David H. Lewis Clinical Research Center, Faculty of Health Sciences, University Hospital, LinkBping, Sweden For the past twenty years or so our research group at the Clinical Research Center in Link~ping Sweden has been studying the effect of various pathophysiologies on the regulation of the microcirculation in a number of organs and tissues. Most of our interest has been focused on skeletal muscle, but studies have also been carried out on skin, myocardium, brain and bone. The pathophysiologies investigated have included: l) hemorrhage and hemorrhagic shock, using various bleeding protocols; 2) trauma including blunt trauma and gun shot wounds with spherical steel missiles; 3) ischemia/reperfusion, including treatment with hyperbaric oxygen. The techniques employed have been virtually exclusively physiologically oriented methodologies aimed at revealing fluid transfer, blood flow patterns in the microcirculation including use of laser Doppler flowmetry and laser Doppler Imaging as well as the hydrogen clearance method, oxygen tension and pH on the surface of the organ and a multitude of parameters of cell metabolism. Studies have been carried out for the most part on anesthetized animals (pigs, rats, rabbits) with many observations in humans as well. Hemorrhage and hemorrhagic shock call forth immediately properly graded compensatory responses which direct the reduced tissue blood flow evenly over the entire capillary network and reduce cell metabolism. The competition between local and central control at the pre-capillary level leads eventually to decompensatory responses, with loss of overall control and death. Trauma is associated with an immediate loss of local control in the traumatized tissue, which does not recover with time. This response, a marked vasodilatatian, resembles an arteriovenous shunt and adds to the circulatory burden, lhe increased blood flow is not related to a healing response on the part of the tissue. The non-traumatized tissues respond in a manner similar to that seen in hemorrhagic shock. With gun shot wounds there is a spectrum of injury from the center of the injured area with dead tissue going out to injured and finally normal tissue. Various treatment methodologies have been employed to reduce the amount of injured tissue that goes toward irreversible injury, but without significant success. Ischemia/reperfusion injury depends on the duration of ischemia with little additional injury due to reperfusion. Ischemia reduces the size of the perfused capillary bed due to injury to endothelial cells and obstruction by adherent leukocytes, which occurs late. The central feature of all these pathophysiologies is loss of microcirculatory control with impaired cell metabolism.
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$5-B1-2-02 PERIPHERAL BLOOD FLOW AND CELL METABOLISM David H. Lewis Clinical Research Center, Faculty of Health Sciences, University Hospital, LinkBping, Sweden For the past twenty years or so our research group at the Clinical Research Center in Link~ping Sweden has been studying the effect of various pathophysiologies on the regulation of the microcirculation in a number of organs and tissues. Most of our interest has been focused on skeletal muscle, but studies have also been carried out on skin, myocardium, brain and bone. The pathophysiologies investigated have included: l) hemorrhage and hemorrhagic shock, using various bleeding protocols; 2) trauma including blunt trauma and gun shot wounds with spherical steel missiles; 3) ischemia/reperfusion, including treatment with hyperbaric oxygen. The techniques employed have been virtually exclusively physiologically oriented methodologies aimed at revealing fluid transfer, blood flow patterns in the microcirculation including use of laser Doppler flowmetry and laser Doppler Imaging as well as the hydrogen clearance method, oxygen tension and pH on the surface of the organ and a multitude of parameters of cell metabolism. Studies have been carried out for the most part on anesthetized animals (pigs, rats, rabbits) with many observations in humans as well. Hemorrhage and hemorrhagic shock call forth immediately properly graded compensatory responses which direct the reduced tissue blood flow evenly over the entire capillary network and reduce cell metabolism. The competition between local and central control at the pre-capillary level leads eventually to decompensatory responses, with loss of overall control and death. Trauma is associated with an immediate loss of local control in the traumatized tissue, which does not recover with time. This response, a marked vasodilatatian, resembles an arteriovenous shunt and adds to the circulatory burden, lhe increased blood flow is not related to a healing response on the part of the tissue. The non-traumatized tissues respond in a manner similar to that seen in hemorrhagic shock. With gun shot wounds there is a spectrum of injury from the center of the injured area with dead tissue going out to injured and finally normal tissue. Various treatment methodologies have been employed to reduce the amount of injured tissue that goes toward irreversible injury, but without significant success. Ischemia/reperfusion injury depends on the duration of ischemia with little additional injury due to reperfusion. Ischemia reduces the size of the perfused capillary bed due to injury to endothelial cells and obstruction by adherent leukocytes, which occurs late. The central feature of all these pathophysiologies is loss of microcirculatory control with impaired cell metabolism.
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