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动脉血栓很少是不在动脉粥样硬化的前提下发生的,损伤后动脉壁的最早的病理学变化之一是平滑肌细胞增生,而这又取决于循环血小板的存在。在这些情况下,白细胞可粘附于内皮,并向释放出致使内皮下膜损伤的微粒体酶的内皮迁移。在血小板和白细胞二者介异的内皮损伤中,内皮下膜被暴露,裸露出胶原。胶原是强烈的血小板粘附刺激剂。然后,血小板即被“激活”,并释放出具有激活花生四烯酸途径的作用的颗粒内容物,即致密颗粒内容物(ADP和5-羟色胺)和α-颗粒内容物(血小板因子4,β-血栓球蛋白和其他),并产生促使进一步聚集的凝血酶。血管损伤亦通过释放凝血激酶或激活因子
Arterial thrombus rarely occurs without atherosclerosis. One of the earliest pathological changes in the arterial wall after injury is smooth muscle cell proliferation, which in turn depends on the presence of circulating platelets. In these cases, leukocytes can adhere to the endothelium and migrate toward the endothelium releasing microsomal enzymes that cause damage to the subendothelial membrane. In an endothelial injury that is both differentiated by platelets and leukocytes, the subendothelial membrane is exposed, exposing to collagen. Collagen is a strong platelet adhesion stimulator. The platelets are then “activated” and release the granulate contents that have the effect of activating the arachidonic acid pathway, namely the dense granule contents (ADP and serotonin) and the a-granule contents (platelet factor 4, beta - thromboxans and others) and produce thrombin that causes further aggregation. Vascular damage is also caused by the release of thromboplastin or activators