Abstract
In arteries of animals with experimental atherosclerosis (Gryglewski et al. 1978, DeGaetano et al. 1979, Larrue et al. 1980, 1982)and in arteries of humans with atherosclerosis (D’Angelo et al. 1978, Sinzinger et al. 1979) or with an exposure to risk factors (Silberbauer et al. 1979, Dadak et al. 1981) the generation of a prostacyclin-like activity is severely suppressed. On the other hand it has been recently reported that the urine excretion of prostacyclin metabolites is augmented in atherosclerosis. The validity of a conception that prostacyclin deficiency is associated with development of atherosclerosis depends on further analytical studies, however, the results of early experimental findings stimulated clinicians to use prostacyclin for treatment of arterial disease (Szczeklik et al. 1979). Irrespectively to a role that prostacyclin may play in pathogenesis of atherosclerosis, the drug itself has a potent platelet-suppressant and vasodilatory actions (Szczeklik et al.,1978). Fibrionolytic (Dembińska-Kieć et al. 1982) and cytoprotective (for ref. see Vane, 1983) properties of prostacyclin might be also of clinical importance.
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Gryglewski, R.J., Szczeklik, A. (1985). Prostacyclin in Therapy of Vascular Disease. In: Samuelsson, B., Berti, F., Folco, G.C., Velo, G.P. (eds) Drugs Affecting Leukotrienes and Other Eicosanoid Pathways. NATO ASI Series, vol 95. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-7841-9_18
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DOI: https://doi.org/10.1007/978-1-4684-7841-9_18
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