Platelet-microvessel interactions.
Platelet-microvessel interactions.
复制标题
血小板-微血管相互作用。
DOI：
10.1080/10739680590925475
复制
发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Rumbaut,RolandoE
中科院分区：
文献类型：
--
作者：
Rumbaut,RolandoE
Platelets are essential for primary hemostasis, and mediate thrombosis in clinical conditions involving macrovessels, such as stroke and myocardial infarction. Platelets also interact with microvessels in various pathophysiologic conditions, though this concept is underemphasized in the literature. The six papers of this issue are devoted to the interactions between platelets and two components of microvessels: endothelium and subendothelium. Molecular mechanisms of platelet adhesion and inhibition of platelet function are reviewed, as well as microvascular models of thrombosis and thromboembolism in vivo. In addition, we review mechanisms of platelet–microvessel interactions in inflammation and the role of blood-borne tissue factor-bearing microparticles in a model of microvascular thrombosis. These contributions provide a general overview of platelet function as well as examples of current areas of active investigation, with the goal of generating interest in the field of platelet–microvessel interactions.This Special Topics issue of Microcirculation is devoted to the interactions of platelets with vascular walls in the microcirculation. Platelets are small (∼ 3× 0.5 µm) discoid anucleated cells, essential for controlling bleeding (hemostasis) at sites of blood vessel injury. In addition to this physiologic role, platelet adhesion and aggregation contribute to important clinical conditions, such as stroke and myocardial infarction. Much of the published research deals with platelet function relevant to these and other macrovascular diseases. In the microcirculation, platelet interactions also occur in a variety of pathophysiologic conditions, though this concept has received much less attention in the literature. As an example, papers published in this journal dealing with leukocytes outnumber those dealing with
