It acts on peripheral nerves, stabilizes nerve tissue cell membranes, reduces sodium ion influx, blocks normal polarization alternation, and prevents nerve impulse transmission, thus playing an analgesic role. Most of it is hydrolyzed and converted by plasma cholinesterase, with an onset time of 2 minutes, Pka8.5 at 25·C, and a maximum dose of 100 mg at a time. Most of the hydrolysis product, p-aminobenzoic acid, is excreted in the urine, and dimethylaminoethanol is further degraded by oxidation, spasm removal, deamination, etc. and is also excreted in the urine: some of it is free or combined with gluconic acid.

This product has anti-inflammatory, antipyretic and analgesic effects. Its mechanism of action is to reduce the synthesis of prostaglandins by inhibiting cyclooxygenase. It stops the formation of pain nerve impulses in inflammatory tissues and inhibits inflammatory reactions, including inhibiting the chemotaxis of leukocytes and the release of lysosomal enzymes. As for the antipyretic effect, it acts on the hypothalamic temperature regulation center, causing peripheral vasodilation and sweating, which increases heat dissipation. This central antipyretic effect may also be related to the inhibition of prostaglandin synthesis in the hypothalamus.

Extract from the above information

Tetracycline antibiotics are broad-spectrum antibacterial agents that specifically bind to the A position of the bacterial ribosome 30S subunit, inhibiting the growth of peptide chains and affecting the synthesis of bacterial proteins. They are sensitive to many Rickettsia, Mycoplasma, Chlamydia, and Spirochete, and are also relatively sensitive to others such as Actinomycetes, Bacillus anthracis, and Listeria monocytogenes, but Enterococci are resistant to them. Common clinical pathogens have serious resistance to oxytetracycline, and there is cross-resistance with other tetracycline antibiotics.

This product is a broad-spectrum antibacterial agent, with bactericidal effect at high concentrations. It has certain antibacterial effects on Streptococcus pneumoniae, hemolytic Streptococcus, Streptococcus viridans and some Staphylococci, Clostridium perfringens, Bacillus anthracis, Yersinia pestis, Corynebacterium diphtheriae, Clostridium tetani, Brucella, Haemophilus influenzae, Campylobacter, Vibrio cholerae, and also has inhibitory effects on Rickettsia, Mycoplasma, Chlamydia, Spirochete, and some protozoa. This product is better than Gram-positive bacteria in effect on Gram-negative bacteria, but Enterococcus is resistant to it. Others such as Actinomyces, Bacillus anthracis, Listeria monocytogenes, Clostridium, Nocardia, etc. are also sensitive to this product. This product has certain antibacterial activity against Neisseria gonorrhoeae and Neisseria meningitidis, but penicillin-resistant gonococci are also resistant to tetracycline. This product has no antibacterial activity against Pseudomonas aeruginosa. It has a certain antibacterial effect on some anaerobic bacteria, but it is far inferior to metronidazole, clindamycin and chloramphenicol, so it is not used clinically. Due to the widespread use of tetracyclines over the years, common clinical pathogens, including Gram-positive bacteria such as Staphylococcus and Gram-negative bacteria such as Enterobacter, have serious tetracycline resistance, and there is cross-resistance between similar varieties. The mechanism of action of this product is that the drug can specifically bind to the A position of the 30S subunit of the bacterial ribosome, preventing the connection of aminoacyl-tRNA at this position, thereby inhibiting the growth of peptide linkages and affecting the synthesis of bacterial proteins.