Platelet–Vessel Wall Interactions

Introduction

Platelets are the sentinels of the circulatory system; they recognize and rapidly respond to a disruption in vascular integrity, thereby preventing significant blood loss. This is achieved through the formation of a primary hemostatic plug, which requires platelets to undergo a highly regulated series of events including the adhesion, activation, generation, and release of thrombogenic agents and ultimately aggregation. The importance of these processes is underscored by the bleeding sequelae that result from a reduction in platelet numbers or function associated with various disease states and complications attributable to invasive monitoring and treatments for critically ill neonates. In fact, a significant proportion of newborns admitted to the neonatal intensive care unit (NICU) will present with or develop thrombocytopenia during their hospitalization. Consequently, an estimated 80,000 platelet transfusions are administered annually to NICU patients in the United States. To complicate matters, neonatal platelets appear to be hyporesponsive to common activating stimuli as compared with those from healthy adults, which may further compromise their ability to adequately support hemostasis. To understand both the mechanisms that may predispose critically ill neonates to bleeding and the clinical relevance of the reported reduction in function of their platelets, it is necessary to have a broad overview of mechanisms that limit as well as promote platelet–vessel wall interactions.

Vascular Endothelium