Dousset J C
Pathol Biol (Paris). 1981 Jan;29(1):53-61.
Endothelial damage results in increased permeability to serum lipoproteins, adhesion of platelets which release a growth - stimulating protein for smooth muscle cells and a number of vasoactive substances, including thromboxanes. Smooth muscle cells migrate from media, proliferate and accumulate lipid. "Atherogenic" lipoproteins enhance arterial accumulation of cholesterol. After infiltration of serum lipoproteins, smooth muscle cells become into lipid - loaded foam cells which die. Cell necrosis produce the amorphous lipid deposits which form the nucleus of the atherosclerosis plaque. The accompanying proliferative and inflammatory response in the developing plaque is associated with increased prostaglandin synthesis. Calcification and ulceration appear. Thromboxane production leads to platelet aggregation and thrombus formation. Antiplatelet and antiinflammatory drugs have beneficial effects by blocking aggregation, inhibiting the vasospasm associated with microthrombus formation and thromboxane release and modifying the inflammatory response by blocking prostaglandin and thromboxane synthesis in the developing plaque.
内皮损伤导致血清脂蛋白通透性增加、血小板黏附，血小板会释放一种刺激平滑肌细胞生长的蛋白质以及多种血管活性物质，包括血栓素。平滑肌细胞从中膜迁移、增殖并蓄积脂质。“致动脉粥样硬化”脂蛋白会增加动脉中胆固醇的蓄积。血清脂蛋白浸润后，平滑肌细胞变成充满脂质的泡沫细胞并死亡。细胞坏死产生无定形脂质沉积，形成动脉粥样硬化斑块的核心。在发展中的斑块中伴随的增殖和炎症反应与前列腺素合成增加有关。出现钙化和溃疡。血栓素的产生导致血小板聚集和血栓形成。抗血小板和抗炎药物通过阻止聚集、抑制与微血栓形成和血栓素释放相关的血管痉挛以及通过阻断发展中的斑块中前列腺素和血栓素的合成来改变炎症反应，从而产生有益作用。
