Abstract
Platelet adhesion in the microcirculation is being reported and studied in a growing number of animal models of human disease. The adhesion molecules utilized by platelets to attach to the walls of microscopic blood vessels have been defined in most model systems, with P-selectin-PSGL-1, GPIIb/IIIa-fibrinogen-ICAM-1, and vWF-GPIbα interactions serving as major adhesion pathways. The binding of platelets to adherent leukocytes appears to contribute significantly to the platelet–vessel wall interactions elicited in many models of disease. Shear forces generated by the movement of blood through the microcirculation exert an important influence on platelet adhesion. Physiologic regulation of platelet adhesion is mediated by both nitric oxide and superoxide, with the former inhibiting and the latter promoting platelet adhesion. The interactions between platelets and the walls of microscopic blood vessels appear to have important implications in the initiation and/or progression of tissue injury associated with different experimental models of human disease.
This work was supported by the National Institutes of Health (P01 DK43785 and R01 DK65649).