Antiaggregants
This information is not intended for purposes of treatment without physician.
Description of the pharmacological group
Antiaggregants (anti-thrombotic medicines)
Antiaggregants include the medicines, which possess the ability to suppress the induced by the damage of the endothelium of vessels aggregation of thrombocytes.
In the clinical practitioner as Antiaggregants they use: the nonselective inhibitors of the ferment of cyclooxygenase - acetylsalicylic acid; the competitory inhibitor of phosphodiesterase - preparation is dipyridamole, the blockers of the ADP- receptors of thrombocytes - ticlopidine, clopidogrel and others
At present acetylsalicylic acid is examined as basic antiaggregant. Preparation possesses the ability to impede the spontaneous and induced aggregation and the adhesion of thrombocytes. At the basis of the mechanism of the action of preparation lies its ability to irreversibly block the activity of the ferment of cyclooxygenase and to thus suppress the synthesis of thromboxane TxA2. An acetylsalicylic acid as antiaggregant in the clinical practice use at the small doses (50- 375 mg in a 24 hour period) - preparations dust devil ASS -50, dust devil ASS -100, aspirin cardio and other this is caused by the fact that at such doses the acetylsalicylic acid suppresses the synthesis of thromboxane TxA2 in the thrombocytes to 90 -98%.
At the basis of the anti-thrombotic action of dipyridamole (sin.: curantil) lies the ability of preparation to increase the content in the thrombocytes cAMP via the blockade of the activity of the ferment of phosphodiesterase and to increase the content in the plasma of the blood of adenosine, which is been the antagonist of natural aggregant ADP.
Mechanism of the anti-aggregative action of the preparation of Ticlopidine (sin.: Ticlid) is caused by the ability of preparation to selectively block the receptors for ADP located on the membrane of thrombocytes, which entails braking the caused by ADP binding of thrombocytes with the fibrinogen and to thus suppress their aggregative activity. Besides this of Ticlopidine stimulates the synthesis of prostaglandins PGD2 and PGE2 and prostacyclin I2 (PGI2), it improves microcirculation. The analogous mechanism of anti-aggregative action possesses the preparation of clopidogrel.
Recently in the clinical to practitioner are inculcated new antiaggregants - abciximab, tirofiban and other at the basis of the mechanism of their action lies the ability of preparations to block so-called GP receptors, located on the cellular membranes of thrombocytes. They assume that the final stage of the aggregation of thrombocytes is precisely with the activation of these receptors connected. Abciximab and close to it of medicines, blocking GP IIb receptors, suppress aggregation of thrombocytes and they thus prevent thrombogenesis.
In the clinical practitioner Antiaggregants use for the preventive maintenance of the thromboses of coronary vessels in patients with the unstable stenocardia and the myocardial infarction, preventive maintenance of thrombosis in patients after coronary artery bypass surgery, operations on the valves of heart, preventive maintenance of thromboses in patients with the atherosclerotic defeat of the vessels of brain, preventive maintenance of venous thromboses and so forth
Antiaggregants are used for treatment of heart failure, hypertension, acute myocardial infarction