Comparative rheology of the adhesion of platelets and leukocytes from flowing blood: why are platelets so small?

We investigated rheological adaptation of leukocytes and platelets for their adhesive functions in inflammation and haemostasis respectively. Adhesion and margination of leukocytes or platelets where quantified for blood perfused through capillaries coated with P-selectin or collagen, when flow rate or suspending phase viscosity, or red cell aggregation or rigidity were modified. Independent variation of shear rate and shear stress indicated that the ability of platelets to attach at higher values than leukocytes was largely attributable to their smaller size reducing their velocity before attachment and especially, drag experienced afterwards. Increasing red cell aggregation increased the number of marginated and adhering leukocytes, but inhibited platelet adhesion without effect on the number marginated. Increasing red cell rigidity tended to inhibit leukocyte adhesion but promote platelet adhesion. The effects on platelets may be explained by changes in the depth of the near-wall, red cell-depleted layer; broadening (or narrowing) this layer to greater (or less) than the platelet diameter would decrease (or increase) the normal force applied by red cells and make attachment less (or more) efficient. Thus, different adhesive capabilities of leukocytes and platelets may arise from their differences in size, both directly because of influence on cell velocity and force experienced at the wall, and indirectly through effects of size on margination in the bloodstream and interaction with the cell-free layer. In addition, red cell aggregation (of hitherto uncertain physiological significance) may be useful in promoting leukocyte adhesion in inflamed venules but inhibiting unwanted platelet deposition in veins.