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Titlebook: Leukotrienes and Prostacyclin; F. Berti,G. Folco,G. P. Velo Book 1983 Springer Science+Business Media New York 1983 Prostaglandin.cancer.i

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Pharmacology of Leukotriene C4 in Guinea-Pig,ions is widely recognized. The recent discovery that some arachidonic acid metabolites, derived from 5-1ipoxigenase pathway, can display potent biological actions which are similar to that of slow reacting substance of anaphylaxis (SRS-A), stimulated a fresh interest in the field of asthma and other
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Inhibition of Arachidonic Acid Metabolism,ons including inflammation, asthma, Bartter’s syndrome, dysmenorrhoea, threatened abortion and premature labour. Thus, compounds which inhibit metabolism of arachidonic acid have a wide therapeutic potential. Additionally, such inhibitors should prove invaluable to the experimental investigator to e
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6-Keto-Prostaglandin E1: Biosynthesis and Circulatory Effects,GI.). Like PGI., 6-keto-PGE. is potent in stimulating renin secretion [l–3], inhibiting platelet aggregation [4], and reducing blood pressure and vascular resistance in diverse regional circulations [5, 6]. In this chaper, we present evidence that 6-keto-PGE. may arise during the course of metabolic
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An , Aggregometer, it is generally accepted that . data does not always reflect . data [2], fewer studies have been undertaken on platelets .. Such, . studies are limited by the cumbersome and invasive nature of existing techniques [3] which has prompted development of a simple, minimally invasive technique for the c
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Inhibition of Platelet Aggregation and Cardiovascular Effect of 5E-13,14-Didehydro Carboprostacyclisive effect in animals and humans [1, 2, 3], many efforts have been made to synthesize PGI.-derivatives that are chemically stable and which possibly have longer lasting action. The first goal has been reached easily enough and carboprostacyclin [4, 5], 10,10-difluoro-13,14-dehydroprostacyclin [6] a
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Clinical Use of Prostacyclin in Vascular Disease,stration of prostacyclin to man [5, 25] and were confirmed in later studies [7, 14]. The action of pros-tacyclin on platelets is manifested in its anti-aggregatory and disaggregatory properties [5, 18, 26]. The former are seen as a marked inhibition of ADP- or collagen-induced platelet aggregation i
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