Tobelem G, Drouet L, Caen J
Nouv Presse Med. 1980 Mar 29;9(15):1081-5.
The role of the blood platelets in the aetiogenesis of arterial lesions has been underlined in recent years by studies of platelet elastase and above all the mitogenic factor of smooth muscle cells. A truly thrombogenic theory of atherosclerosis can now be envisaged. In the context of arterial thromboses, it is interaction between the damaged vessel wall, the lesion most often being atherosclerosis, and blood platelets which gives rise to the thrombus. In certain conditions such as diabetes abnormalities in the interaction between platelets and vessel walls may favour the development of vascular lesions and thromboses. With regard to venous thrombosis, the participation of the vessel and/or platelets is less clear. However, recently described platelet procoagulant activities could activate coagulation mechanisms. Knowledge of diseases of primary haemostasis has benefited from studies of platelet-vessel interaction. Whilst the spontaneous haemorrhagic syndrome of major thrombocytopaenia remains mysterious, platelet membrane molecular abnormalities in thrombopathies such as Bernard Soulier syndrome or thrombasthenia offer an explanation for their mechanisms. By their interaction with the vessel, platelets finally participate in mechanisms of inflammation, immunological conflicts, disseminated intravascular coagulation and metastatic dissemination.
近年来，通过对血小板弹性蛋白酶尤其是平滑肌细胞促有丝分裂因子的研究，血小板在动脉病变发病机制中的作用得到了凸显。如今可以设想出一种真正的动脉粥样硬化血栓形成理论。在动脉血栓形成的情况下，受损的血管壁（病变最常见的是动脉粥样硬化）与血小板之间的相互作用会导致血栓形成。在某些情况下，如糖尿病，血小板与血管壁之间相互作用的异常可能会促进血管病变和血栓形成的发展。关于静脉血栓形成，血管和/或血小板的参与情况尚不清楚。然而，最近描述的血小板促凝血活性可能会激活凝血机制。对原发性止血疾病的认识受益于对血小板 - 血管相互作用的研究。虽然严重血小板减少症的自发性出血综合征仍然神秘，但诸如伯纳德·索利尔综合征或血小板无力症等血小板病中的血小板膜分子异常为其发病机制提供了解释。通过与血管的相互作用，血小板最终参与炎症、免疫冲突、弥散性血管内凝血和转移扩散等机制。
