White J G
Department of Laboratory Medicine, University of Minnesota Medical School, Minneapolis 55455.
Eur J Clin Invest. 1994 Feb;24 Suppl 1:25-9. doi: 10.1111/j.1365-2362.1994.tb02422.x.
Despite the broad array of mechanisms designed to protect the endothelial lining of every blood vessel in the body and maintain the fluid state of blood, injury does occur. Chronic and recurrent damage result in development of lesions characteristic of atherosclerosis. The loss of vascular integrity associated with the pathological process of atherogenesis triggers the haemostatic mechanism. As a result, fibrin and platelets become a part of atherosclerotic lesions and play a role in their progression. Growth of the plaques and destruction of normal endothelium triggers further involvement of platelets leading to occlusion of arteries in the heart and brain, resulting in myocardial infarction and stroke. Understanding the role of platelets in atherosclerosis and limiting its contribution may reduce morbidity and mortality of this dread disease.
尽管存在一系列旨在保护人体每条血管内皮并维持血液流体状态的机制，但损伤仍会发生。慢性和复发性损伤会导致动脉粥样硬化特征性病变的发展。与动脉粥样硬化发生的病理过程相关的血管完整性丧失会触发止血机制。结果，纤维蛋白和血小板成为动脉粥样硬化病变的一部分，并在其进展中发挥作用。斑块的生长和正常内皮的破坏会引发血小板的进一步参与，导致心脏和大脑中的动脉阻塞，从而引发心肌梗死和中风。了解血小板在动脉粥样硬化中的作用并限制其影响，可能会降低这种可怕疾病的发病率和死亡率。
