Adhesive interactions between leukocytes and platelets can be demonstrated in the flowing blood or at the vessel wall, where immobilised platelets may capture leucocytes. Platelets may bind to matrix proteins exposed after damage to endothelium or to intact endothelial cells exposed to a variety of stimuli. When covering large areas, platelets support a rolling form of adhesion by all types of leukocytes, and even small numbers of platelets may briefly capture flowing cells. In the case of activated neutrophilic granulocytes, platelets can also support their immobilisation and migration. Platelets themselves may supply the neutrophil-activating signal. The molecular basis of the adhesive interactions have been well described, and from the rheological point of view, the flow rates and shear stresses at which interaction can occur have been defined in models using purified cells. However, it is not clear under what conditions such interactions can occur in whole blood, especially in the context of arterial flow where pulsatility and discontinuities in the wall may be predicted to greatly influence deposition of these cells. Animal models suggest that codeposition can occur in arteries, and an understanding of how this comes about could significantly contribute to our understanding of atherosclerosis and of thrombotic complications, for example, associated with reconstructive surgery or angioplasty.