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Dipyridamole inhibits platelet phosphodiesterase, causing an increase in cyclic AMP with potentiation of the action of PGI 2 – opposes actions of TXA 2 Epoprostenol is a prostacyclin that is used to inhibit platelet aggregation during renal dialysis (with or without heparin) and is also used in primary pulmonary hypertension.
Glycoprotein IIb/IIIa inhibitors are frequently used during percutaneous coronary intervention (angioplasty with or without intracoronary stent placement). They work by preventing platelet aggregation and thrombus formation. They do so by inhibition of the GpIIb/IIIa receptor on the surface of the platelets.
Aggregation of platelets is highly regulated by cyclic nucleotides. PDE3A is a regulator of this process, and PDE3 inhibitors effectively prevent aggregation of platelets. Cilostazol is approved for treatment of intermittent claudication and is thought to involve inhibition of platelet aggregation and also inhibition of smooth muscle ...
By adding methylsulfanylethylamino group at the C4 position and trifluoropropylsulfanyl at the chainlength leads to the formation of the drug cangrelor that has enhanced activity. Cangrelor has a 78% mean recovery of ADP induced platelet aggregation in rat after 20 minutes comparison to compound 1C which has a less than 10% recovery. [22]
Platelet aggregation function by disorders and agonists ADP Epinephrine Collagen Ristocetin; P2Y receptor defect [1] (including Clopidogrel) Decreased: Normal: Normal: Normal Adrenergic receptor defect [1] Normal: Decreased: Normal: Normal Collagen receptor defect [1] Normal: Normal: Decreased or absent: Normal Von Willebrand disease (except ...
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The underlying mechanism for the deleterious effect proposes that endothelial cells lining the microvasculature in the body express COX-2, whose selective inhibition results in levels of prostaglandin I2 (PGI2, prostacyclin) down-regulated relative to thromboxane (since COX-1 in platelets is unaffected).
The complex is formed via calcium-dependent association of gpIIb and gpIIIa, a required step in normal platelet aggregation and endothelial adherence. [ 2 ] [ 3 ] Platelet activation by ADP (blocked by clopidogrel ) leads to the aforementioned conformational change in platelet gpIIb/IIIa receptors that induces binding to fibrinogen. [ 1 ]