Abstract
At the time of the discovery of prostacyclin(PGX,PGI2) we also reported that its biosynthesis had been inhibited by 15-HPETE and by “a mixture of peroxides which were non-enzymically formed from arachidonic acid11”, A hypothesis was put forward that “a reduction in the amount of those lipid peroxides which inhibit the generation of PGX,... would be of considerable significance in preventing the development of atherosclerosis and arterial thrombosis”1.An experimental evidence was soon presented that a high lipid diet fed to rabbits had caused an increase in plasma lipid pegojcides and a suppression of the generation of prostacyclin by arteries 2–4. In human athegogclerotic lesions the generation of prostacyclin was also suppressed 5,6.
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© 1988 Plenum Press, New York
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Gryglewski, R.J., Kostka-Trabka, E., Dembinska-Kiec, A., Korbut, R. (1988). Prostacyclin and Atherosclerosis -Experimental and Clinical Approaches. In: Malmendier, C.L., Alaupovic, P. (eds) Eicosanoids, Apolipoproteins, Lipoprotein Particles, and Atherosclerosis. Advances in Experimental Medicine and Biology, vol 243. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0733-4_3
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