Abstract
The in vivo production of prostacyclin (PGI2) in man is normally very low. The use of specific analytical methods has shown that the concentration of PGI2 in peripheral blood is less than 3 pg/ml (10 pM), a concentration too low to inhibit platelets (Blair et al., 1982). The measurement of the main urinary metabolite of PGI2, prostaglandin 2,3-dinor-6-keto F1α, has allowed to estimate that the rate of PGI2 secretion into the circulation of normal man is ± 0.1 ng/kg × min, whereas studies with exogenous PGI2 suggest that infusion rates of 2–4 ng/kg × min are required to achieve the threshold for inhibition of platelet function (FitzGerald et al., 1981). Several diseases involving the intravascular activation of platelets are associated with an increased biosynthesis of PGI2 which might represent a compensatory mechanism : severe atherosclerosis of the lower limbs (FitzGerald et al., 1984), systemic sclerosis complicated by Raynaudfs phenomenon (Reilly et al., 1986), unstable angina, during the episodes of chest pain and acute myocardial infarction (Fitzgerald et al., 1986).
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© 1988 Plenum Press, New York
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Boeynaems, J.M. et al. (1988). Control of Prostacyclin Production by Vascular Cells : Role of Adenine Nucleotides and Serotonin. 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_2
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DOI: https://doi.org/10.1007/978-1-4613-0733-4_2
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