Translational Therapeutics of Dipyridamole — Volkswagen Polo Vivo

17 Июн 2015 | Author: | Комментарии к записи Translational Therapeutics of Dipyridamole — Volkswagen Polo Vivo отключены
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Dipyridamole (DP) is a inhibitor that increases the levels of cyclic adenosine (cAMP) and cyclic guanine (cGMP) by preventing their to AMP and GMP, respectively. By increasing and cGMP levels in platelets, DP inhibits platelet aggregation and thrombotic disease. In addition, DP may some of the vascular protective of endothelium-derived nitric oxide which increases cGMP by soluble guanylyl cyclase. NO is an important regulator of vascular blood flow, and tissue Indeed, endothelial NO synthase-deficient −/− ) mice exhibit elevated blood pressure and have myocardial and cerebral infarct after ischemic injury. NO/cGMP-dependent effects that may be by DP include inhibition of vascular muscle proliferation and prevention of interaction. In addition, DP increases concentrations of adenosine and prostacyclin, could affect vascular and inflammation. Finally, DP has antioxidant which could stabilize and vascular membranes as well as the oxidation of low-density lipoprotein. platelet and nonplatelet actions of DP may to some of its therapeutic benefits in disease.


This article is of a multi-part CME-certified activity Translational Therapeutics at the Platelet Interface. In order to achieve all of the learning objectives, please all of the components of the activity listed in the of Contents and follow the “Instructions for and Obtaining CME Credit” outlined to the Introduction .

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Antiplatelet therapy such as (ASA) has been the cornerstone for the of cardiovascular disease, particularly strokes. However, the relatively magnitude of benefits derived aspirin monotherapy, ie, 14% to 20% relative (RR) reduction compared placebo, has spurred the search for effective antiplatelet agents or 1–3 Surprisingly, the Management of Atherothrombosis Clopidogrel in High-Risk Patients and Clopidogrel for High Atherothrombosis and Ischemic Stabilization, Management, and (CHARISMA) studies indicate the addition of another antiplatelet, to ASA does not confer additional for secondary strokes compared ASA or clopidogrel alone. 4,5 Bleeding however, were increased this combination. In contrast, of dipyridamole (DP) to ASA in the European Prevention Study (ESPS)-2 and the Stroke Prevention in Reversible Trial (ESPRIT) reduced the RR of by about 20% compared with ASA

without incurring excess 6,7 Surprisingly, the risk of bleeding was with DP plus ASA compared ASA alone. These findings that DP may exert vascular effects beyond platelet

Adenosine and Platelet Inhibition

DP was found to increase extracellular of adenosine by inhibiting adenosine by red blood cells, thereby to inhibition of platelet aggregation 1 ). 8 Adenosine is released from wall cells and platelets the extracellular space as a breakdown of adenosine triphosphate (ATP). adenine nucleotides are rapidly to adenosine by nucleases. In circulating free adenosine is rapidly from plasma by a specific carrier into red blood At clinically relevant doses, DP adenosine uptake by red blood by 90% and increases plasma adenosine by 60%. 9,10 Adenosine, through adenosine receptors, adenylyl cyclase in platelets and intracellular levels of cyclic monophosphate (cAMP), which is a inhibitor of platelet activation. 11 It be noted that DP can also intracellular levels of cAMP in by preventing the breakdown of cAMP via of phosphodiesterase (PDE). 12,13 DP has been shown to inhibit aggregation in whole blood in

and potentiate the antiaggregatory effect of in vitro. 14,15

Volkswagen Polo Vivo
Volkswagen Polo Vivo
Volkswagen Polo Vivo

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