Moncada S, Gryglewski R, Bunting S, Vane J R
Nature. 1976 Oct 21;263(5579):663-5. doi: 10.1038/263663a0.
Microsomes prepared from rabbit or pig aortas transformed endoperoxides (PGG2 or PGH2) to an unstable substance (PGX) that inhibited human platelet aggregation. PGX was 30 times more potent in this respect than prostaglandin E1. PGX contracted some gastrointestinal smooth muscle and relaxed certain isolated blood vessels. Prostaglandin endoperoxides cause platelet aggregation possibly through the generation by platelets of thromboxane A2. Generation of PGX by vessel walls could be the biochemical mechanism underlying their unique ability to resist platelet adhesion. A balance between formation of anti- and pro-aggregatory substances by enzymes could also contribute to the maintenance of the integrity of vascular endothelium and explain the mechanism of formation of intra-arterial thrombi in certain physiopathological conditions.
从兔或猪主动脉制备的微粒体将内过氧化物（PGG2或PGH2）转化为一种抑制人血小板聚集的不稳定物质（PGX）。在这方面，PGX的效力比前列腺素E1强30倍。PGX使一些胃肠平滑肌收缩，并使某些离体血管舒张。前列腺素内过氧化物可能通过血小板生成血栓素A2而导致血小板聚集。血管壁生成PGX可能是其抵抗血小板黏附的独特能力的生化机制。酶形成抗聚集物质和促聚集物质之间的平衡也可能有助于维持血管内皮的完整性，并解释在某些生理病理条件下动脉内血栓形成的机制。
