The effects of erythrocyte aggregation on O(2) release were examined using O(2)-permeable fluorinated ethylenepropylene copolymer tubes (inner diameter, 25 microm; outer diameter, 100 microm). Measurements were performed using an apparatus built on an inverted microscope that contained a scanning-grating spectrophotometer with a photon count detector connected to two photomultipliers and an image processor through a video camera. The rate of O(2) release from the cells flowing in the narrow tube was determined based on the visible absorption spectrum and the flow velocity of the cells as well as the tube size. When the tube was exposed to nitrogen-saturated deoxygenated saline containing 10 mM sodium dithionite, the flowing erythrocytes were deoxygenated in proportion to the traveling distance, and the deoxygenation at a given distance increased with decreasing flow velocity and cell concentration (hematocrit). Adding Dextran T-70 to the cell suspension increased erythrocyte aggregation in the tube, which resulted in suppressed cell deoxygenation and increased marginal cell-free-layer thickness. The deoxygenation was inversely proportional to the cell-free-layer thickness. The relation was not essentially altered even when the medium viscosity was adjusted with Dextran T-40 to remain constant. The rate of O(2) release from erythrocytes in the tube was discussed in relation to the O(2) diffusion process. We conclude that the diffusion of O(2) from erythrocytes flowing in narrow tubes is inhibited primarily by erythrocyte aggregation itself and partly by thickening of the cell-free layer.

Flow dynamics of human erythrocytes was compared in elastic (E) and hardened (H) microvessels with inner diameters of 10-40 microns. The thickness of the marginal cell-free layer and the overall flow resistance were measured with a vascular bed isolated from rabbit mesentery (E vascular bed) as well as with a 4% paraformaldehyde-fixed bed (H vascular bed). 1) In both E and H microvessels, the thickness of the cell-free layer increased with increasing inner diameter of the microvessels and with decreasing hematocrit accompanied by an overall decrease in the flow resistance. The hematocrit-dependent change of the cell-free layer thickness was greater in the E microvessels than in the H microvessels. The flow resistance was always greater in the H vascular beds than in the E vascular beds. 2) With decreasing erythrocyte deformability induced by treatment with 2 mM diazenedicar-boxylic acid bis(N,N-dimethylamide), the thickness of the cell-free layer decreased at a low hematocrit in the E microvessels and at a high hematocrit in the H microvessels, although the flow resistance was increased in both vascular beds. 3) Dextran of 70,400 average molecular weight accelerated the formation of the cell-free layer by inducing erythrocyte aggregation. A drastic increase in the cell-free layer thickness at 2-4 g/dl of dextran in the E microvessels and at 1-2 g/dl of dextran in the H microvessels was accompanied by a significantly lower increase in the flow resistance. This study concludes that the elasticity of microvessels may play an important role for reducing the overall flow resistance of a vascular bed, which is modulated by the marginal cell-free layer, itself a function of the rheological properties of the erythrocytes.

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Effects of erythrocyte aggregation on the flow dynamics of erythrocytes in microvessels were examined quantitatively by perfusing human erythrocytes suspended in isotonic medium containing various concentrations of dextran (70,400 avg mol wt, Dx-70) into a part of the microvascular bed isolated from rabbit mesentery. Thickness of the marginal cell-free layer was measured with an image analyzer, total flow resistance was determined on the basis of the perfusion pressure-volume flow relationship, and homogeneity of erythrocyte flow was evaluated by the power spectrum obtained by the fast Fourier transform of the light intensity change monitored on single microvessels. With increasing dextran concentration, suspension viscosity of erythrocytes at high shear rates increased linearly and thickness of the cell-free layer increased in a sigmoidal fashion. Flow resistance increased relatively little over the range of dextran concentrations in which the cell-free layer increased most rapidly. Furthermore, the flow pattern of erythrocytes in microvessels became inhomogeneous. In conclusion, the present study shows that Dx-70-induced erythrocyte aggregation results in increased flow resistance in the circulatory system, even through the widening of the cell-free layer tends to reduce the resistance and also results in inhomogeneous flow of erythrocytes in microvessels.

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