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自70年代发现血栓素A_2和前列环素后,前列腺素对心血管系统作用显著改观。在血小板中,花生四烯酸主要转变成血栓素A_2不稳定的血管收缩剂(半寿期30sec)和血小板聚集物。在血管壁,花生四烯酸却被转变成前列环素——不稳定的血管扩张剂(半寿期2～3min)和抗聚集物。前列环素的主要性能是保护血管壁免受血小板聚集物的沉积。大血管壁合成前列环素的能力,在血管内膜表面最大。内皮细胞是前列环素最活跃的制造者,任何细胞膜的变形都会引起前列环素的释放。每次心跳时心包壁层和脏层的牵拉,也可导致前列环素的释放,在心包壁层和脏层间起着润滑作用。前列环素的第三种活性是细胞保护作用,在实验性心肌梗塞中,静脉输注前列环素有抗心
Since the discovery of thromboxane A 2 and prostacyclin in the 1970s, the effects of prostaglandins on the cardiovascular system have been significantly improved. In platelets, arachidonic acid is mainly converted to thromboxane A 2 unstable vasoconstrictor (half-life of 30 sec) and platelet aggregates. On the walls of the blood vessels, arachidonic acid is converted to prostacyclin - an unstable vasodilator (half-life 2 to 3 minutes) and anti-aggregates. The main property of prostacyclin is to protect the walls of blood vessels from the accumulation of platelet aggregates. The ability of the large blood vessel wall to synthesize prostacyclin is greatest at the intima surface. Endothelial cells are the most active manufacturers of prostacyclin, and any deformation of the cell membrane causes the release of prostacyclin. Stretching the parietal and visceral layers during each heartbeat can also lead to the release of prostacyclin, which acts as a lubricant between the parietal and visceral layers of the pericardium. The third activity of prostacyclin is a cytoprotective effect. In experimental myocardial infarction, intravenous prostacyclin is resistant