Analysis of the effects of measured white blood cell entrance times on hemodynamics in a computer model of a microvascular bed

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Abstract
To quantify the interdependence of capillary leukocyte plugging and microvascular hemodynamics, experimental measurements were made of the time required for lymphocytes and granulocytes to enter a micropipette. Using standard micropipette deformation techniques, entrance times were found to be a function of both cell diameter and pipette diameter, with no significant dependence on aspiration pressure over the differential pressure range of 200–400 Pa. Experimental results were combined with a computer network model to describe changes in red cell distribution and flow rate resulting from the delayed entrance of leukocytes (WBC) into capillaries. The network model is based on geometrical measurements from the capillary bed of a hamster cremaster muscle (Sarelius et al. 1981) and utilizes previous work describing: 1. preferential cell distribution at a bifurcation, 2. increased apparent viscosity due to the presence of red and white cells, and 3. increased velocities of red and white cells relative to blood. Red and white cell positions within the network were computed at discrete time increments, and WBC plugging was simulated by a temporary cessation of flow in vessels of smaller diameter than the white cell. In contrast with previous studies, the increased viscosity due to the presence of WBCs was found to have an insignificant effect on overall network flow rate. Instead, a major flow reduction occurs only when capillaries are plugged by the white cells. At normal physiological concentrations (1,000 RBC/WBC), time-averaged overall network flow is reduced by 4.4%, based on averaged experimentally measured entrance times, and up to 14.8% if maximal entrance times are used. Overall flow rates fluctuate significantly with time and, at concentrations greater than 1 WBC/200 RBC, decrease substantially with increasing WBC concentration. At levels comparable to acute leukemia (70 RBC/WBC), flow is severely compromised due to numerous WBC occlusions. In the absence of WBCs, mean hematocrit and hematocrit distribution compare well with published values. Spatial variations in hematocrit are notable, however, and capillaries originating from the upstream end of the arteriole have a much lower hematocrit than downstream branches (by a factor of two, on average) due to preferential distribution of red blood cells.