Pharmacological action of acetylsalicylic acid
Aspirin is the first antiplatelet drug used in antithrombotic therapy, and has been established as a classic drug for the treatment of acute myocardial infarction (AMI), unstable angina and secondary prevention of myocardial infarction (MI). The principle of action is that aspirin can cause COX inactivation through irreversible acetylation with the hydroxyl group of serine residue at 530 position of polypeptide chain in COX-1 active site of cyclooxygenase (COX), and then block the conversion of AA to thromboxane A2 (TXA2), thus inhibiting PLT aggregation.
COXs are the key rate limiting enzymes in the process of AA producing TXA2 and prostaglandin I2 (PGI2). There are two forms of COX-1 and COX-2 in the human body. COX-1 is inherent in PLT. Clinical studies have shown that short-term or long-term aspirin treatment for patients with various ischemic cardiovascular and cerebrovascular diseases and other high-risk groups has clear benefits in preventing possible subsequent myocardial infarction, stroke, and vascular death, but there are still disputes on the optimal dose and aspirin resistance. With the development of antiplatelet aggregation drug research, the main clinical problem is to determine the laboratory monitoring indicators of the efficacy and side effects of antiplatelet aggregation drugs.
① Analgesic effect: mainly through inhibiting the synthesis of prostaglandins and other substances (such as bradykinin and histamine) that can make pain sense sensitive to mechanical or chemical stimuli, it belongs to peripheral analgesic drugs. However, the possibility of central analgesia (possibly acting on the hypothalamus) cannot be ruled out;
② Anti inflammatory effect; The exact mechanism is still unclear. It may be that the product acts on inflammatory tissues, and plays an anti-inflammatory role by inhibiting the synthesis of prostaglandins or other substances that can cause inflammatory reactions (such as histamine). It may also be related to the inhibition of lysosomal enzyme release and leukocyte activity;
③ Antipyretic effect: It may play an antipyretic effect by acting on the hypothalamic thermoregulatory center to cause peripheral blood vessel expansion, increase skin blood flow, sweat, and increase heat dissipation. This central effect may be related to the inhibition of prostaglandin synthesis in the hypothalamus;
④ Anti rheumatism effect: the anti rheumatism mechanism of the product is mainly anti-inflammatory, in addition to antipyretic and analgesic effects;
⑤ Inhibition of platelet aggregation: It works by inhibiting the prostaglandin cyclooxygenase of platelets, thus preventing the formation of thromboxane A2 TXA2 (TXA2 can promote platelet aggregation). This action is irreversible. 
The absorption is rapid and complete after oral administration. It has begun to be absorbed in the stomach, and most of it can be absorbed in the upper part of the small intestine. The absorption rate is related to the solubility and pH of gastrointestinal tract. Food can reduce the absorption rate, but does not affect the absorption amount. Enteric coated tablets absorbed slowly. This product can be absorbed quickly when taken with sodium bicarbonate. After absorption, it is distributed in various tissues and can also penetrate into joint cavity and cerebrospinal fluid. The protein binding rate of aspirin is low, but the protein binding rate of salicylate after hydrolysis is 65~90%. The binding rate decreased when the blood concentration was high. Poor renal function and low delivery rate during pregnancy. The half-life is 15-20 hours; The half-life of salicylate depends on the dosage and urine pH, and it takes about 2-3 hours to take a small dose at a time; It can last more than 20 hours in large dosage and 5~18 hours in repeated administration. The half-life of salicylate in milk after a single oral administration of 0.65g aspirin is 3.8-12.5 hours. Most of the product is quickly hydrolyzed into salicylate in the gastrointestinal tract, liver and blood, and then metabolized in the liver. The metabolites are mainly salicyluric acid and glucuronic acid conjugates, and a small part is oxidized to gentic acid. The blood drug peak value was reached 1-2 hours after one dose. The blood drug concentration during analgesia and antipyretic is 25-50 μ g/ml； 150~300 for anti dampness and anti inflammation μ g/ml。 The time required for the blood drug concentration to reach a stable state increases with the increase of daily dose and blood drug concentration, and can be as long as 7 days in the case of large dose medication (such as anti rheumatism). For patients with long-term high-dose medication, as the main metabolic pathway of the drug has been saturated, a slight increase in the dose can lead to a large change in the blood concentration. The product is mostly excreted from the kidney as a combined metabolite and a small part as free salicylic acid. The excretion of unmetabolized salicylic acid increases when the dosage is large. There can be great differences between individuals. The pH of urine has an effect on the excretion rate. The excretion rate is accelerated in alkaline urine, and the amount of free salicylic acid is increased, but the opposite is true in acidic urine.
The product can be excreted in milk. Lactating women take 650mg orally. After 5-8 hours, the drug concentration in milk can reach 173-483 μ G/ml, so infants may have adverse reactions when long-term high-dose medication is used.