thromboxane A2


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thromboxane A2 (TXA2)

[thrombok′sān]
biologically active compound derived from prostaglandin G2 with a 30-second half-life. It increases in concentration after injury to blood vessels and stimulates the primary hemostatic response and irreversible platelet aggregation.

thromboxane A2

(throm-bok'san),

TXA2

An unstable compound synthesized in platelets and other cells from a prostaglandin, PGH2. It acts to aggregate platelets, is a potent vasoconstrictor, and mediates inflammation.
See: eicosanoid; prostaglandin; prostanoids
References in periodicals archive ?
Thromboxane A2 receptor antagonism by flavonoids: structure-activity relationships.
Picotamide: It is a combined inhibitor of thromboxane A2 synthase and receptor and, at variance with aspirin, does not interfere with endothelial prostacyclin (PGI2) production.
Oxygen free radicals rise, thromboxane A2 and adhesion molecules are activated, platelet aggregation occurs and vascular vasoconstriction activity is increased.
Plasma levels of thromboxane A2 on admission are associated with no-reflow after primary percutaneous coronary intervention.
Lu-Suguro et al utilized guinea pigs and found glucosamine decreased platelet aggregation in response to ADP by 51% and this study also prevented ADP-induced extracellular release of ATP and thromboxane A2 production by 91% and 96%, respectively.
3) Aspirin and clopidogrel represent current standard antiplatelet agents blocking platelet cyclooxygenase-1 and thromboxane A2.
Nitric oxide, Bradykinin, Prostacyclin, Serotonin, Histamin, Substance P and Endothelium- derived hyperpolarizing factor are the vasodilators while the substances like Angiotensin, Endothelin (ETI), Thromboxane A2, Serotonin, Arachidonic acid, Prostaglandin H2 and Thrombin are the vasoconstrictor molecules released by the endothelium (16).
COX-2 inhibitors suppress endothelial production of prostacyclin, leaving prothrombotic platelet thromboxane A2 mediated by COX-1 relatively unopposed.
5) Aspirin blocks the synthesis of thromboxane A2 from arachidonic acid in platelets by inhibiting the enzyme cyclooxygenase 1 (Figure 1).
It reduces the formation of an inflammatory messaging molecule known as thromboxane A2 as well.
It irreversibly inhibits platelet cyclooxygenase, a key enzyme in prostaglandin synthesis, so platelets lose the capacity to synthesize thromboxane A2, an inducer of platelet aggregation with vasoconstrictive properties.
Baynas Tablet is an agent that antagonizes prostaglandin D2 and thromboxane A2 receptors, which cause allergic rhinitis.