Indications for antiplatelet purpose: Coronary heart disease, unstable angina, myocardial infarction, secondary prevention of myocardial infarction after coronary artery bypa*s state, rheumatic heart disease, transient and acute cerebrovascular events, prevention of cerebral infarction, peripheral vascular disease, membranous- proliferative nephritis, diabetic microangiopathy; phlebothrombosis.Acetylsalicylic acid (aspirin).Antiplatelet effect of aspirin is shown in the irreversible inhibition of cyclooxygenase in platelets, which leads to reduced formation of thromboxane A2 in them and lose their ability to aggregate.Aspirin affects platelets before reaching the systemic circulation, ie in the portal vein, where aspirin has not yet been presystemic metabolism.In the systemic circulation aspirin (depending on dose) comes in very small quantities and generally present a metabolite that does not affect platelet cyclooxygenase and the vascular wall, which is synthesized prostacyclin.Such pre-emptive effect on platelets is manifested in the use of low-dose aspirin (50-80 mg / day), higher doses might be more inhibits the synthesis of prostacyclin in the vascular wall.Due to the irreversible effects on platelets antiplatelet effect of aspirin does not correlate with T1 / 2, and it can be administered 1 time per day.Sometimes, this property is undesirable, particularly in the development of side effects such as hemorrhage, then even after the drug effect still lasts a few days.INDOBUFEN (ibustrin).Differs from aspirin fast onset of effect and reversibility of the effects on cyclooxygenase, which creates a controlled antiplatelet effect.Oral bioavailability is high (90%); T1 / 2 is 7-8 hours completely metabolized in the liver and excreted by the kidneys as inactive metabolites.Loading dose - 200 mg 2 times a day, supporting - 100-200 mg once a day.In elderly patients the dose is reduced to 100 mg.Sulfinpyrazone (anturan) is weaker than aspirin for antiplatelet action.High bioavailability (90%); T1 / 2 - about 2-4 hours Not metabolized (less than 10%) and 85% is excreted by the kidneys unchanged.May enter into a drug-drug interactions, competing for active transport in renal tubules with other NSAIDs, furosemide, digoxin, aminoglycosides.Assign to 400 mg 2 times a day.Ticlopidine (tiklid).Causes a dose-dependent antiplatelet effect.Inhibits platelet adhesion, decreases platelet aggregation, prevents the formation fibrinogenovyh bridges between platelets and inhibits mezhtrombotsitarnye interaction.The effect is manifested at 4 days after the appointment, reaching a peak after 8-11 days, be terminated 14 days after cancellation.The drug is inactive (prodrug).After metabolism in the liver produces about 20 metabolites, which are found in urine and plasma.Tmax - 2 h, T1 / 2
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