Abstract
It has been shown originally by Moncada et al. (1976) that prostacyclin (PGI2), a new metabolite of the arachidonic acid (20:4) metabolism, is formed by vascular tissue. This new prostaglandin has been demonstrated to be the most potent known inhibitor of platelet aggregation (Gryglewski et al. 1976) and a very strong vasodilator. In their original paper Moncada et al. (1976) pointed out that only vascular endothelium forms prostacyclin which was the base for their hypothesis that an intact endothelial lining prevents mural platelet thrombus formation. Later, Moncada et al. (1977), Hornstra et al. (1977) and Silberbauer et al. (1978) found using different methods that the endothelial lining is the main source of PGI2, but subendothelial and medial tissue generate prostacyclin too.
This investigation was supported by the Atherosclerosis and Thrombosis Research Commission of the Austrian Academy of Sciences.
The PGI2-standard was kindly provided by Dr. John E. Pike.
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Sinzinger, H., Silberbauer, K., Auerswald, W. (1980). Prostacyclin Production by Vascular Smooth Muscle and Endothelial Cells. In: Gotto, A.M., Smith, L.C., Allen, B. (eds) Atherosclerosis V. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-6071-4_29
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DOI: https://doi.org/10.1007/978-1-4612-6071-4_29
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