INTRODUCTION

The recent view of platelets as simply cellular fragments involved in hemostasis has gradually changed with the growing awareness of the multiple physiologic roles of platelets. There is growing evidence of the role platelets play in the immune system, where they act as part of the innate immune system in their response to infection. Platelet granules are also rich in vasoactive and inflammatory mediators such as adenosine diphosphate (ADP) and serotonin, growth factors, and cytokines. Even the view of platelets as cellular fragments has changed. Although platelets do not contain a nucleus, they do contain mRNA, which is transcribed into active products when the platelet is activated.

Drug therapy is designed to alter either platelet number or platelet function. For the purpose of pharmacologic intervention, platelets have three functions: adhesion, secretion, and aggregation. Damage to the endothelial cell layer provides a thrombogenic surface that allows platelets to adhere. This is accompanied by activation of the platelet, which results in its degranulation (secretion). Many of the secreted agents are biologically active and can lead to further platelet activation (e.g., secreted ADP). This recruits further platelets, forming an aggregate.

Platelet adhesion is mediated by different interactions that are dependent on the shear conditions (i.e., static, low, or high shear conditions).