Both acute and chronic phases of vascular disease are associated with a stress response that includes increased hepatic synthesis of fibrinogen and increased bone marrow release of leucocytes and platelets. A likely humoral mediator of the stress response is interleukin-1 released by reticulo-endothelial cells following their stimulation by fibrinogen degradation fragments D and E. Rheological consequences of the stress response include hyperviscosity of plasma and whole blood and decreased blood filterability. Since blood filterability is influenced by both the plasma fibrinogen concentration and the leucocyte count, it is essential to completely remove these extrinsic contaminants by a pre-filtration step before a true measurement of erythrocyte deformability can be made. Understanding of the pathogenesis of these stress syndromes is also a prerequisite to successful therapeutic control of the rheological abnormality of vascular disease.