It can dilate blood vessels and improve microcirculation

This product is a semi-synthetic 14-membered macrolide antibiotic. Its antibacterial spectrum and antibacterial effect are basically similar to those of erythromycin. Its effect on Gram-positive bacteria is slightly worse than that of erythromycin, and its effect on Legionella pneumophila is stronger than that of erythromycin. Its antimicrobial effect on Chlamydia pneumoniae, Mycoplasma pneumoniae, and Ureaplasma urealyticum is similar to or slightly stronger than that of erythromycin. This product can penetrate the bacterial cell membrane and reversibly bind to the 50S subunit of the bacterial ribosome near the donor (P position), blocking the transfer RNA (t-RNA) from binding to the P position, and also blocking the transfer of the polypeptide chain from the acceptor position (A position) to the P position, thereby inhibiting bacterial protein synthesis.

Omeprazole is a racemic mixture of a pair of active optical enantiomers. It reduces gastric acid secretion through a highly targeted mechanism of action and is a special inhibitor of the acid pump in gastric parietal cells. This product acts rapidly, and a once-daily dose can reversibly inhibit gastric acid secretion. Omeprazole is a weakly alkaline substance that is concentrated and converted into active substances in the highly acidic environment of the tubules in gastric parietal cells, inhibiting H, K-ATPase (proton pump). This inhibitory effect on the final step of gastric acid formation is dose-related, and highly inhibits basal gastric acid secretion and irritant gastric acid secretion, but has nothing to do with irritants. Intravenous administration of omeprazole in humans inhibits gastric acid secretion in a dose-related manner. In order to quickly achieve the same effect of reducing gastric acidity as multiple oral administrations of 20 mg, it is recommended to give 40 mg of omeprazole intravenously for the first time. Intravenous injection of 40 mg of omeprazole rapidly reduces gastric acidity, with an average decrease of 90% within 24 hours. The inhibitory effect of omeprazole on gastric acid secretion is related to the area under the drug-time curve (AUC), but has nothing to do with the blood drug concentration at the time of administration. Omeprazole combined with antibiotics can eradicate Helicobacter pylori, which is associated with rapid relief of symptoms, high rates of gastric mucosal repair, and long-term remission of peptic ulcer disease, thereby reducing complications such as gastrointestinal bleeding and the need for long-term treatment with anti-acid drugs.

It acts directly on the endogenous fibrinolytic system, catalyzing the cleavage of plasminogen into plasmin, degrading fibrin clots, fibrinogen in the blood circulation, coagulation factor V and coagulation factor VIII, etc., to exert a thrombolytic effect; it increases the activity of vascular ADP enzyme, inhibits ADP-induced platelet aggregation, and prevents thrombosis; it increases the activity of plasmin in the patient's body, reduces the increase in plasma fibrin or fibrinogen levels and their degradation products; it shows that the thrombolytic effect is related to the drug dosage and the time window of administration; it may increase the risk of severe bleeding.

It acts directly on the endogenous fibrinolytic system, catalyzing the cleavage of plasminogen into plasmin, degrading fibrin clots, fibrinogen in the blood circulation, coagulation factor V and coagulation factor VIII, etc.; it has a rapid onset and good effect on newly formed thrombi; it increases the activity of vascular ADP enzyme, inhibits ADP-induced platelet aggregation, and prevents thrombosis; it increases the activity of plasmin in the patient's body; it reduces the level of plasma fibrin or fibrinogen and increases its degradation products; the thrombolytic effect is related to the drug dose and the time window of administration; it has low toxicity, and has no obvious antigenicity, teratogenicity, carcinogenicity, and mutagenicity.