Shattil S J, Bennett J S
Ann Intern Med. 1981 Jan;94(1):108-18. doi: 10.7326/0003-4819-94-1-108.
Platelets form a plug and promote thrombin generation at sites of vascular injury. These processes are initiated by interaction of the platelet plasma membrane with various substances within or accumulating at the injured vessel. Thus, platelet adhesion to exposed subendothelium requires the binding of von Willebrand factor to platelets. Agonists such as thrombin bind to membrane receptors, thereby stimulating the binding of fibrinogen to platelets and resulting in the aggregation of platelets onto those already adherent to the vessel wall. Agonists also stimulate transfer of membrane=bound calcium into the cytoplasm. This triggers the secretion of granule substances and results in the recruitment of additional platelets to the hemostatic plug. Concomitant with secretion, the platelet surface supports several reactions leading to thrombin generation. Thus, hemostasis requires a series of coordinated responses involving platelet membranes. A defect in any of these responses can lead to a bleeding diathesis.
血小板在血管损伤部位形成栓子并促进凝血酶生成。这些过程由血小板质膜与受损血管内或在受损血管处积聚的各种物质相互作用引发。因此，血小板与暴露的内皮下层的黏附需要血管性血友病因子与血小板结合。凝血酶等激动剂与膜受体结合，从而刺激纤维蛋白原与血小板结合，导致血小板聚集到已黏附于血管壁的血小板上。激动剂还刺激膜结合钙转移到细胞质中。这触发颗粒物质的分泌，并导致更多血小板募集到止血栓中。伴随分泌过程，血小板表面支持多种导致凝血酶生成的反应。因此，止血需要一系列涉及血小板膜的协调反应。这些反应中任何一个出现缺陷都可能导致出血素质。
