Circulating leukocytes and platelets must adhere to the wall of blood vessels in order to carry out the protective function of immunity for leukocytes and hemostasis for platelets: failure or lack of control in recruitment can be pathogenic. Given the importance of these adhesive processes, it is not surprising that they have been widely studied both in vivo using intravital microscopy and in vitro using flow-based models. It has become increasingly recognized that adhesion is constrained by the local hemodynamic environment and modulated by the rheological properties of the blood. The rate of motion of the cells before capture and the shear forces acting on them during adhesion critically control the efficiency of attachment. The rheology of the blood influences these hemodynamic parameters. It also affects the efficiency with which cells are brought into contact with the wall because margination in the flow depends on the concentration of the red cells and their flow-dependent tendency to aggregate [1]. Thus, physiological and pathological mechanisms of leukocyte and platelet adhesion represent important rheological phenomena requiring understanding at the biomechanical as well as molecular-biological levels.

Flow-based studies have revealed that in each case, leukocytes and platelets use a multi-step process to achieve controlled recruitment [2, 3]. Broadly, specialized receptors support capture of fast-moving cells, separate receptors support stable attachment, and activating signals are required for transition between the states. The actual substrates and receptors differ; leukocytes usually adhere to intact endothelium while platelets typically adhere to sub-endothelial matrix exposed in damaged vessels. In the case of leukocytes, attachment is followed by migration through the endothelium, while platelets undergo spreading and an aggregation phase, and act as a surface for coagulation and fibrin deposition. Leukocyte adhesion is mainly restricted to post capillary venules where shear rates and stresses are relatively low. However, platelet adhesion is possible in all vessels in order to inhibit blood loss, and can occur in arteries at much higher shear rates and stresses. Clearly, there are interesting parallels but important distinctions between the behaviors of the two cell types.

Here we review basic concepts of dynamic cellular adhesion and experimental approaches to their investigation that are largely common between the platelets and leukocytes. The specific mechanisms underlying adhesion in the vascular system are then described for the different cells, and the major physico-chemical modulators of adhesion are outlined. Finally, ways in which abnormal adhesive responses can contribute to pathology are considered with particular attention to how these might influence blood circulation.