19th Meeting of the Japanese Society of Biorheology
407
EFFECTS OF RED CELL AGGREGATION AND SEDIMENTATION ON THE TUBE HEMATOCRIT T. Murata Department of Physics, Tokyo Metropolitan University, Tokyo, Japan When blood flows through narrow tubes with diameters less than about 300um, the hematocrit in the tube HT is always lower than the hematocrit of the blood exiting from the tube HD. This phenomenon has first been described by Fahraeus and is now called the Fahraeus effect. The Fahraeus effect is explained by a nonuniform distribution of the flowing red blood cells across the tube. On the other hand it is known that human red blood cells form aggregates in whole blood flowing through tubes at low flow rates. Microscopic observations of flow field of aggregating red cell suspensions in narrow vertical tubes have shown that aggregated red cells form an almost uninterrupted cell column in the axis of the stream. In horizontal tubes red cell aggregates settle to a lower tube wall under the influence of gravity. The sedimentation of red cell aggregates leads to a non&symmetric cell distribution. Therefore, formation of aggregates in blood flowing through a tube substantially affects the distribution of red cells acrossthe tube cross-section. The purpose of this study is to estimate theoretically the effects of red cell aggregation and sedimentation on the Fahraeus effect using two mathematical flow models developed in our previous papers. One consists of a cylindrical core of aggregated red cells and plasma surrounding the core that is eccentrically located in a horizontal long tube. It is assumed that the cylindrical core moves as a rigid body along the tube axis. This is the flow model for red cell suspensions with the higher aggregation tendency. ‘lbe other model consists of plasma in the upper part of the tube and a concentrated red cell suspension in the bottom part divided by a smooth and horizontal interface. It is assumed that the suspension is a Newtonian fluid whose viscosity increasesexponentially with hematocrit. This is the flow model for red cell suspensions with the lower aggregation tendency. The relative hematocrit HT/HD is calculated as a function of some parameters that characterize the geometry of red cell aggregate. From the theoretical results and the experimental data of Reinke et al. (1987) HT/HD is given as a function of pseudo-shear rate.
HEMATOCRIT DEPENDENCE OF CELL-FREE LAYER THICKNESS IN CAT CEREBRAL ARTERIOLES: AN INTRAVITAL FLUORESCENCE MICROSCOPIC OBSERVATION Hussain. M.A.. Yamakawa. T. and Niimi. H. Dept. of Microcirculatory Science, National Cardiovascular Center Research Institute, Suita, Osaka, Japan Cell-free layer appears at the endothelial wall of microvessels. Since cellular interactions in whole blood influence cell-free layer, the hematocrit may govern the mode and extent of such interactions. To see the correlation of cell-free layer with hematocrit in viva, we studied the cell-free layer change in cat cerebral arterioles under increasing hematocrit. Cats were anesthetized, artificially ventilated and surgically operated for a cranial window. Both side femoral arteries and veins were cannulated using polyethylene tubes for isovolemic blood exchange. The hematocrit was measured during the experiment using microtube technique. An intravenous injection of RITC-labeled dextran and FITC-labeled red cells provided fluorescence images of the arteriolar lumen and red cell column respectively. The observations and recordings were made using a fluorescence microscope. The diameters of the red cell column and microvessel were measured in 5 arterioles based on the video-images (RITC, FITC). The thickness of the cell-free layer was calculated as half of the difference between the two diameters. Red cell velocity was measured using a dual-window technique. The pseudo shear-rate was calculated by the ratio of the red cell velocity to the microvessel diameter. The observed microhemodynamic changes included arteriolar dilatation and a decreasein the red cell velocity. The cell-free layer thickness increased with hemoconcentration. The mean arterial pressure decreased by 11.4% of the mean control value at the final stage of hemoconcentration. The present analysis showed: 1) The cell-free layer thickness increased linearly with a decreasein the shear-rate, p< 0.001. 2) The change in cell-free layer thickness for a given change in shear-rate at hemotocrit ~45% was greater than at hematocrit ~45%. 3) The mean red cell velocity decreasedlinearly with decreasing shear-rate (p< 0.001).