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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 ...
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).
For many years dual treatment with the cyclooxygenase-1 (COX-1) inhibitor aspirin and clopidogrel was routine practice and served as the main antiplatelet agents for the prevention of thrombotic events as they have the capability to powerfully manipulate platelet biology, which plays a central part in thrombosis.
Disintegrins work by countering the blood clotting steps, inhibiting the clumping of platelets.They interact with the beta-1 and -3 families of integrins receptors. . Integrins are cell receptors involved in cell–cell and cell–extracellular matrix interactions, serving as the final common pathway leading to aggregation via formation of platelet–platelet bridges, which are essential in ...
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 ]
These agonists induce platelet adhesion, activation and aggregation, leading to rapid occlusion of the aperture and cessation of blood flow termed the closure time (CT). An elevated CT with EPI and collagen can indicate intrinsic defects such as von Willebrand disease, uremia, or circulating platelet inhibitors.