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  • thromboxane
  • Thromboxane-A synthase , an enzyme found in platelets , converts the arachidonic acid derivative prostaglandin H 2 to thromboxane. (wikipedia.org)
  • These "Sticky platelets" secrete several chemicals, including thromboxane A2 that stimulate vasoconstriction, reducing blood flow at the site. (wikipedia.org)
  • The widely used drug aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets. (wikipedia.org)
  • Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H2, and therefore thromboxane A2. (wikipedia.org)
  • Thromboxane synthesis inhibitors, in turn, can be classified regarding which step in the synthesis they inhibit: The widely used drug aspirin acts by inhibiting the ability of the COX enzyme to synthesize the precursors of thromboxane within platelets. (wikipedia.org)
  • vessel
  • If the cap of a vulnerable plaque erodes or ruptures, as in MI, platelets stick to the damaged lining of the vessel and to each other within seconds and form a plug. (wikipedia.org)
  • A number of agonists, generated at the interface between the vessel wall and circulating blood at the site of vascular injury, have been shown to activate platelets. (aspetjournals.org)
  • The process includes the following steps: Following damage to the blood vessel, FVII leaves the circulation and comes into contact with tissue factor (TF) expressed on tissue-factor-bearing cells (stromal fibroblasts and leukocytes), forming an activated complex (TF-FVIIa). (wikipedia.org)
  • thrombus formation
  • Platelet adhesion/thrombus formation in the endocardium was found in limited sites in which the overlying endothelium was deficient in eNOS and CD34. (onlinejacc.org)
  • When warfarin-treated cases were excluded, there was a significant correlation between the immunohistochemical grade for vWF and the degree of platelet adhesion/thrombus formation in the endocardium. (onlinejacc.org)
  • GPVI
  • Recent biochemical and cellular studies on shedding pathways 7-10 and surface expression 11-13 of GPVI illustrate some of the key mechanisms underlying platelet receptor proteolysis, and recent preclinical studies 14 show how significant these findings may be in the context of thrombotic risk. (ahajournals.org)
  • antithrombotic
  • Together, the findings may be broadly applicable to other cell types, and may provide new approaches for antithrombotic therapies or assessment of thrombotic risk. (ahajournals.org)