Streptozotocin 18883-66-4 processes by blocking the signals of proteins derived

Rse of several hours. 7 Thus, k Blutpl Streptozotocin 18883-66-4 can play Ttchen an R The infl ammation, angiogenesis and wound healing, and antiplatelet therapy k Can influence these processes by blocking the signals of proteins derived from platelets for infl ammatory reaction or proliferating. Negative modulation of adhesion Commission and Blutpl Ttchen aggregation by a variety of physiological mechanisms, including normal endothelium-derived prostacyclin, nitric oxide, ADPase and CD39/ecto Blutpl Ttchen endothelial Zelladh Exercised sion molecule first Some medications k Can interfere with these regulatory pathways, as a dose-ed exemplifi Independent inhibition of PGI 2 production by aspirin and other COX-1 and COX 2 inhibitors. 3The article about therapy with antiplatelet agents by the American College of Chest Physicians Evidence-Based Clinical Practice Guidelines examines the anticoagulant effect of non-stero Dian traditional antiinfl ammatory drugs and the kardiovaskul Ren Effects of COX-2 selective NSAIDs. This topic is not covered here, and interested readers are invited to the previous article. 8 1.0 Aspirin Aspirin is the drug at the h Ufigsten studied antiplatelet drug. Based on. 100 randomized trials in patients at high risk, reduced vascular aspirin Mortality Ren t by 15% and not t Dlichen vascular Ren events by 30%. 9.10 1.1 The best characterized mechanism of action mechanism of the effect of aspirin is its F Ability, the activity t of F inhibit searches Is permanent COX prostaglandin H synthase 1 and prostaglandin H synthase second COX isozymes catalyze the 15th November fi rst step in the biosynthesis of prostano Of, arachidonic acid conversion To prostaglandin H 2 PGH 2 is the immediate precursor of TXA 2 and PGI second The molecular mechanism of inhibition of COX activity stable t with aspirin binds to COX-channel blockers by acetylation of serine residue of a strategic position, it prevents access to the catalytic site of the enzyme substrate. 16 A completely Requests reference requests getting completely or almost Requests reference requests getting inhibition of platelet COX-1, with low doses of aspirin once t Possible to achieve. In contrast, require the inhibition of COX-2 dependent Ngigen pathophysiological processes h Higher doses of aspirin and the dosage interval is much shorter, since nucleated cells rapidly resynthesize the enzyme. Thus, Ben 10 h to 100 times Her daily doses of aspirin Firmed when the drug as a means antiinfl ammatory like t as a Antipl Ttchen funds will be used. The benefit / risk benefit of aspirin is dose- Because of its gastrointestinal toxicity ngig t is dose- Dependent. To human platelets and endothelial cells process PGH 2 to produce primarily TXA 2 and PGI 2. 12 TXA 2 induces PI Ttchenaggregation and vasoconstriction, w While PGI 2 inhibits platelet aggregation and induces vasodilation. 12 Since TXA 2 is largely derived from COX-1, it is very sensitive to inhibition by aspirin. However, although vascular Ren PGI 2 may be derived from COX-1 is also the major source of COX-2, even under Idarubicin 57852-57-0 physiological conditions. 17 COX-1 dependent Independent PGI 2 production were with Hnlichen rates of MI, stroke or kardiovaskul Rem associated death. 47 The ASA and carotid endarterectomy trial revealed that the risk of stroke, MI or death within 3 months of carotid endarterectomy was lower fa Signifi cant for patients receiving aspirin or 81 325 mg / day than in those of the 650 or 1300 mg / d 46th.