White J G
Cardiovasc Clin. 1987;18(1):13-33.
The leading cause of mortality in industrialized societies is sudden cardiac death. Almost half a million people die each year in the United States from myocardial ischemia and infarction leading to ventricular fibrillation. These phenomena result from severe coronary artery disease due to atherosclerosis with acute mural thrombosis causing occlusion, which serves as the terminal event. Various studies have found evidence of fresh coronary artery mural thrombosis in 74 to 94 percent of patients undergoing autopsies shortly after death due to acute myocardial infarction. Not all thrombi are occlusive, but vasospasm associated with fresh injury to the diseased vessel may be sufficient with developing new thrombus to block blood flow. Because platelets are a major constituent of newly formed thrombi and contribute significantly to vaso-occlusive disease, it is important to understand basic aspects of their function. Such studies may lead to measures that prevent vascular disease and thrombosis. This chapter has described ultrastructural features of platelet-vessel wall interaction. Adhesion, spreading, secretion, and aggregate or thrombus formation have been emphasized. The findings of current studies indicate strong similarities between platelet-vessel wall interactions and the response of platelets to other surfaces. Also, platelet transformations observed during aggregate formation in suspension are identical to physical changes in thrombi on damaged vessels. The similarities are much more impressive than the differences. Therefore, the role of platelets in arterial thrombosis can be understood best as an extension of their hemostatic function. An advantage of this observation is that understanding basic mechanisms of platelet function in hemostasis can lead to solution of the problems presented by platelet involvement in thrombosis. The disadvantage is that agents used to prevent thrombosis can place the hemostatic mechanism in jeopardy. Finding the answer to this paradox will occupy our attention for years to come.
工业化社会中主要的死亡原因是心源性猝死。在美国，每年有近50万人死于心肌缺血和梗死导致的心室颤动。这些现象是由动脉粥样硬化引起的严重冠状动脉疾病导致的，急性壁血栓形成导致血管闭塞，这是最终事件。各种研究发现，在因急性心肌梗死死亡后不久接受尸检的患者中，74%至94%的人有新鲜冠状动脉壁血栓的证据。并非所有血栓都会导致血管闭塞，但与病变血管新损伤相关的血管痉挛，可能足以与新形成的血栓一起阻断血流。由于血小板是新形成血栓的主要成分，并且对血管闭塞性疾病有显著影响，因此了解其功能的基本方面很重要。此类研究可能会带来预防血管疾病和血栓形成的措施。本章描述了血小板与血管壁相互作用的超微结构特征。重点强调了黏附、铺展、分泌以及聚集或血栓形成。当前研究结果表明，血小板与血管壁的相互作用和血小板对其他表面的反应之间有很强的相似性。此外，在悬浮液中聚集形成过程中观察到的血小板变化与受损血管上血栓的物理变化相同。相似之处比差异更为显著。因此，血小板在动脉血栓形成中的作用最好被理解为其止血功能的延伸。这一观察结果的优点是，了解血小板在止血中功能的基本机制可以解决血小板参与血栓形成所带来的问题。缺点是用于预防血栓形成的药物可能会危及止血机制。找到这个矛盾的答案将在未来几年吸引我们的关注。
