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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.

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