Sinzinger H, Wasinger T
Atherosclerosis Research Group, Vienna, Austria.
Z Kardiol. 1989;78 Suppl 6:30-4.
Prostaglandin 12, a potent antiplatelet agent, is formed by arterial wall cells to a differing extent. Various mechanisms are involved regulating synthesis and degradation. The mechanisms by which PGI2 exerts its biological action are still under debate. The most prominent ones are the action on fibrinolysis, thromboresistance, smooth muscle cell proliferation, extracellular matrix formation, endothelial stability, lipid metabolism, cytoprotection, and white blood cells among others. In vivo investigations have proven some of these mechanisms in human. The decreased thrombogenicity, endothelial stabilization, and reduction in intravascular lipids can be visualized under gamma-camera after autologous labelling of platelets or LDL, respectively. The local interaction of eicosanoids with other compounds regulates hemostasis in a rather complex system.
前列腺素12是一种强效抗血小板剂，由动脉壁细胞在不同程度上生成。涉及多种调节合成和降解的机制。前列环素（PGI2）发挥其生物学作用的机制仍在争论中。最突出的机制包括对纤维蛋白溶解、抗血栓形成、平滑肌细胞增殖、细胞外基质形成、内皮稳定性、脂质代谢、细胞保护和白细胞等的作用。体内研究已在人体中证实了其中一些机制。分别对血小板或低密度脂蛋白（LDL）进行自体标记后，在γ相机下可以观察到血栓形成性降低、内皮稳定和血管内脂质减少。在一个相当复杂的系统中，类花生酸与其他化合物的局部相互作用调节止血。
