Journal ArticleDOI
Effects of a selective inhibitor of thromboxane synthetase on human blood platelet behaviour
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TLDR
It is shown that at concentrations similar to those required to inhibit thromboxane synthesis, UK-34787 inhibited arachidonate-induced aggregation and release reaction in platelet rich plasma from some, but not all, individuals.About:
This article is published in Thrombosis Research.The article was published on 1980-10-15. It has received 85 citations till now. The article focuses on the topics: Thromboxane & Thromboxane-A synthase.read more
Citations
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The central role of the P(2T) receptor in amplification of human platelet activation, aggregation, secretion and procoagulant activity.
Robert F. Storey,Heather M. Sanderson,A. N. N. E. White,Jane A. May,Kathryn E. Cameron,Stan Heptinstall +5 more
TL;DR: It is indicated that the P2T receptor plays a central role in amplifying platelet responses and demonstrate the clinical potential of P2 T receptor antagonists.
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Differential inhibition by low-dose aspirin of human venous prostacyclin synthesis and platelet thromboxane synthesis.
TL;DR: The long-lasting effect of 300 mg aspirin on both venous tissue and platelets indicates that this dose is unlikely to produce a favourable prostacyclin/thromboxane balance.
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Prostacyclin and thromboxanes. Implications for their role in tumor cell metastasis.
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Endogenous prostacyclin biosynthesis and platelet function during selective inhibition of thromboxane synthase in man.
TL;DR: Evidence for a platelet-inhibitory effect of the compound was a significant prolongation of the bleeding time at 1 h after administration of the highest dose (200 mg) of dazoxiben.
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Gingerols and related analogues inhibit arachidonic acid-induced human platelet serotonin release and aggregation.
TL;DR: The results provide a basis for the design of more potent synthetic gingerol analogues, with similar potencies to aspirin, as platelet activation inhibitors with potential value in cardiovascular disease.
References
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Journal ArticleDOI
Thromboxanes: a new group of biologically active compounds derived from prostaglandin endoperoxides.
TL;DR: Evidence is presented that the more unstable and major component of rabbit aorta contracting substance (RCS) formed in platelets and guinea pig lung is also thromboxane A2.
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Isolation and Structure of Two Prostaglandin Endoperoxides That Cause Platelet Aggregation
TL;DR: Platelet aggregation induced by thrombin was accompanied by release of material reducible by stannous chloride into prostaglandin F(2alpha), thus indicating the involvement of endogenous prostaglandsin endoperoxides in platelet aggregation.
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Unstable metabolites of arachidonic acid and their role in haemostasis and thrombosis
S Moncada,J R Vane +1 more
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Physiological role of an endoperoxide in human platelets: hemostatic defect due to platelet cyclo-oxygenase deficiency.
TL;DR: It is concluded that the endoperoxide (PGG2) is essential in normal hemostasis because of its role in initiating the release reaction required for aggregation by collagen and the second wave of aggregation caused by, e.g., ADP.
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Prostaglandin D2 inhibits the aggregation of human platelets
TL;DR: Prostaglandin D2, heretofore considered to be biologically inactive, was found to be more than twice as potent as prostaglandsin E1 as an inhibitor of aggregation in human citrated platelet-rich plasma.