[Biochemistry of atherogenesis: effects of prostaglandins (author's transl)]

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.