The high splenic hematocrit: a rheological consequence of red cell flow through the reticular meshwork.

The spleen concentrates blood to twice arterial hematocrit, but how it does so is poorly understood. We hypothesize that hemoconcentration results from percolation of blood through the reticular meshwork (RM) between capillary endings and venous channels. The RM has a large flow cross section, producing low shear rates, and an enormous surface area for red blood cell (RBC) adhesion. If these conditions cause slowing of RBCs with respect to plasma, increased hematocrits will occur (inverse Fahraeus effect). Movements of individual RBCs through the RM were studied from intravital microscopic videorecordings of Ringer-perfused mouse spleens. Analysis of three 70-microns paths showed characteristic "stop and go" motion, RBCs spending 0.015 to 9.71 see in any 7-microns segment, despite steady (+/- 15%) perfusate velocity. At some locations RBCs adhered to reticular cells/fibers by point attachment and at others they became caught over fibers. In general, RBCs were detained in the RM by surface interactions rather than by narrow channel. Perfusate ("plasma") velocity was estimated to be at least that of the fastest RBCs in each segment. Ratios of overall mean RBC and plasma velocities for three paths were 0.19, 0.20, and 0.37. Applying these velocity ratios to a feed hematocrit of 40% leads to predicted splenic hematocrits up to 78%. We conclude that this slowing of RBCs within the reticular meshwork provides the primary mechanism for generating the high intrasplenic hematocrit.