Larrue J, Rigaud M, Daret D, Demond J, Durand J, Bricaud H
Nature. 1980 Jun 12;285(5765):480-2. doi: 10.1038/285480a0.
Prostacyclin (PGI2) synthesis seems to be one of the major physiological mechanisms involved in regulating platelet and vessel wall interactions. PGI2 is produced in large amounts by vascular endothelial cells, and vascular smooth muscle cells (SMC) also produce significant quantities. The capacity of SMC to produce PGI2, especially after endothelial injury, seems to be of importance. It is probably this type of situaton that is involved in the atherosclerotic process: experimental atherosclerosis in rabbits has been associated with a severe decrease in PGI, synthesis by arteries. Lipid peroxide accumulation within the arterial wall or in the plasma may also be involved in this process. Using arterial SMC in culture, we demonstrate here that, in comparison with healthy cultured cells, cells originating from atherosclerotic aorta have a decreased capacity to produce PGI2. The results were obtained using biological and radiochemical techniques and were confirmed by GC-MS. They suggest a potential role for PGI2 in inhibiting the atherosclerotic process.
前列环素（PGI2）的合成似乎是调节血小板与血管壁相互作用的主要生理机制之一。血管内皮细胞大量产生PGI2，血管平滑肌细胞（SMC）也能产生相当数量的PGI2。SMC产生PGI2的能力，尤其是在内皮损伤后，似乎具有重要意义。可能正是这种情况参与了动脉粥样硬化过程：兔实验性动脉粥样硬化与动脉PGI2合成的严重减少有关。动脉壁内或血浆中脂质过氧化物的积累也可能参与此过程。我们在此利用培养的动脉SMC证明，与健康培养细胞相比，源自动脉粥样硬化主动脉的细胞产生PGI2的能力降低。结果通过生物学和放射化学技术获得，并经气相色谱-质谱法（GC-MS）证实。这些结果表明PGI2在抑制动脉粥样硬化过程中可能发挥作用。
