thromboxane


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thromboxane

 [throm-bok´sān]
an intermediate in the metabolic pathway of arachidonic acid, formed from prostaglandin endoperoxides, and released from suitably stimulated platelets; the unstable form, thromboxane A2, is a potent inducer of platelet aggregation and constrictor of arterial smooth muscle.

throm·box·ane

(throm-bok'sān),
The formal parent of the thromboxanes; prostanoic acid in which the -COOH has been reduced to -CH3 and an oxygen atom has been inserted between carbons 11 and 12.

thromboxane

/throm·box·ane/ (-bok´sān) either of two compounds, one designated A2 and the other B2. Thromboxane A2 is synthesized by platelets and is an inducer of platelet aggregation and platelet release functions and is a vasoconstrictor; it is very unstable and is hydrolyzed to thromboxane B2.

thromboxane

(thrŏm-bŏk′sān)
n.
Any of several compounds, originally derived from prostaglandin precursors in platelets, that stimulate aggregation of platelets and constriction of blood vessels.

thromboxane

any of several compounds synthesized by platelets and other cells that cause platelet aggregation and vasoconstriction.

thromboxane (thrôm·bôkˑ·sān),

n one of a pair of compounds that effectively induces platelet aggregation.

thromboxane

an intermediate in the metabolic pathway of arachidonic acid, formed from prostaglandin endoperoxides, and released from suitably stimulated platelets; the unstable form, thromboxane A2, is a potent inducer of platelet aggregation and constrictor of arterial smooth muscle.
References in periodicals archive ?
1984) Prostacyclin and thromboxane synthase as P450 enzymes.
Authors stated previous research that "Prostaglandin E2 is involved in the classic signs of inflammation and possesses both pro-inflammatory and anti-inflammatory actions; thromboxane A2, formed by platelets, macrophages and polymorphonuclear leukocytes, can induce vasoconstriction and promotes aggregation of platelets as well as adhesiveness of polymorphonuclear neutrophils; leukotriene B4 (LTB4) can not only increase vascular permeability and enhance local blood flow by stimulating neutrophil secretion, but also stimulate other inflammatory substances.
Vollaard, A comparison of the effects of nabumetone vs meloxicam on serum thromboxane B2 and platelet function in healthy volunteers, British Journal of Clinical Pharmacology, 53(6), 644-647 (2002).
2+] levels [63], inhibits thromboxane receptors in platelets [64], and diminishes platelet recruitment in thrombus formation [65].
Several studies in different populations have shown protective mechanisms for risk with the association of low doses of calcium plus linoleic acid by improving the balance between thromboxane A2/prostaglandin E2, by reducing intracellular free calcium, by antagonizing the activity of the renin-angiotensin-aldosterone, by reducing the endothelial dysfunction, and by reversing the metabolic syndrome (5,6); which has not been observed with calcium supplementation alone (8).
These include the significance of the balance between prostacyclin and thromboxane [A.
Aspirin plays a crucial physiological and pathophysiological role in cardiovascular diseases and cerebrovascular diseases by irreversibly inhibiting thromboxane A2.
Compared to smaller platelets, larger platelets have more granules, aggregate more rapidly with collagen, have higher thromboxane A2 level, and express more glycoprotein Ib and IIb/IIIa receptors.
The EPA and DI-IA of omega-3 fatty acids become prostaglandins, while omega-6 fatty acids include arachidonic acid (AA), which moves through the pathway to become a thromboxane.
Omega-6 fatty acids are commonly thought to be pro-inflammatory, because linoleic acid (the major omega-3 fatty acid in the diet) is converted in part to arachidonic acid, which is a precursor for pro-inflammatory eicosanoids such as prostaglandin E2, leukotriene B4, and thromboxane A2.
26] TST also induces a hyper-coagulable state via increases in thromboxane A[sub.
3] by aspirin [acetylsalicylic acid (ASA)] and the consequent attenuation of thromboxane [A.