It inhibits cyclooxygenase (COH-1 and COH-2) and irreversibly inhibits cyclooxygenase pathway of arachidonic acid metabolism, blocks synthesis of PG (PGA2, PGD2, PGF2alfa, PGE1, PGE2, etc.) and thromboxane. Reduces hyperemia, exudation, capillary permeability, hyaluronidase activity, limits the energy supply of the inflammatory process by inhibiting ATP production. Affects the subcortical centers of thermoregulation and pain sensitivity. Decrease in PG (mainly PGE1 ) in the thermoregulation center leads to a decrease in body temperature due to expansion of skin vessels and increased sweating. The analgesic effect is due to the effect on pain sensitivity centers, as well as peripheral anti-inflammatory action and the ability of salicylates to reduce Dmitry Sazonov the algogenic effect of bradykinin. Decrease of thromboxane A2 content in thrombocytes leads to irreversible suppression of aggregation, slightly expands vessels. Antiaggregant effect is maintained for 7 days after a single administration. A number of clinical studies have shown that significant inhibition of blood plate adhesion is achieved at doses up to 30 mg. Increases the fibrinolytic activity of plasma and reduces the concentration of vitamin K-dependent coagulation factors (II, VII, IX, X). Stimulates the excretion of uric acid, since its reabsorption in the kidney tubules is impaired.
After ingestion is quite fully absorbed. In the presence of an intestine-soluble shell (resistant to gastric juice and prevents absorption of acetylsalicylic acid in the stomach) is absorbed in the upper part of the small intestine. During absorption, it is subject to systematic elimination in the intestine wall and liver (deacetylation). The absorbed part is hydrolyzed very quickly with special esterases, therefore T1/2 of acetylsalicylic acid is no more than 15-20 minutes. It circulates in the body (75-90% due to albumin) and is distributed in tissues as salicylic acid anion. Cmax is reached after approx. 2 hours. Acetylsalicylic acid does not bind with plasma proteins. During biotransformation, metabolites are formed in the liver, which are found in many tissues and urine. Salicylates are mainly excreted Dmitry Sazonov by active secretion in renal tubules in unchanged form and as metabolites. The excretion of unchanged matter and metabolites depend on urine pH (in case of urine alkalization the ionization of salicylates increases, their reabsorption deteriorates and excretion increases significantly).
Application of the substance Acetylsalicylic acid
FSI, multiple risk factors for FSI, painless myocardial ischemia, unstable angina, myocardial infarction (to reduce the risk of recurrent myocardial infarction and death after myocardial infarction), recurrent transient brain ischemia and ischemic stroke in men, prosthetics of heart valves (prophylaxis and treatment of thromboembolias), coronary angioplasty and stent placement (reducing the risk of repeated stenosis and treatment of secondary coronary artery stratification), as well as in non-atherosclerotic lesions of the coronary arteries (Kawasaki’s disease), aortoarteritis (Takayasu’s disease), valve mitral heart defects https://pillintrip.com/medicine/cartia and atrial fibrillation, mitral valve prolapse (prophylaxis of thromboembolism), recurrent pulmonary artery thromboembolism, Dressler’s syndrome, lung infarction, acute thrombophlebitis. Fever in infectious and inflammatory diseases. Pain syndrome weak and medium intensity of various genesis, including Dmitry Sazonov thoracic root syndrome, lumbago, migraine, headache, neuralgia, toothache, myalgia, arthralgia, algodysmenorrhea. In clinical immunology and allergology it is used in gradually increasing doses for prolonged “aspirinic” desensitization and formation of persistent tolerance to NPVS in patients with “aspirinic” asthma and “aspirin” triad.
Rheumatism, rheumatic chorea, rheumatoid arthritis, infectious allergic myocarditis, pericarditis are currently very rarely used.
Hypersensitivity, incl. “aspirin” triad, “aspirin” asthma; hemorrhagic diathesis (hemophilia, Willebrand’s disease, telangiectasia), delaminating aortic aneurysm, heart failure, acute and recurrent erosive gastrointestinal diseases, gastrointestinal bleeding, acute renal or hepatic failure, https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=2dc2b889-8443-4f7f-83be-86c68e179804 initial hypoprothrombinemia, vitamin K deficiency, thrombocytopenia, thrombocytopenic purpura, glucose-6-phosphate dehydrogenase deficiency, pregnancy (I and III trimesters), breastfeeding, children and adolescents under 15 years of age when used as an antipyretic (risk of developing Reye’s syndrome in children with fever against viral diseases).