Sulfonamides are the earliest type of artificially synthesized broad-spectrum antibacterial drugs used. The minimum effective concentration in the blood is 5 mg/100 ml, and 10-15 mg/100 ml is required for severe infections. They are effective against most Gram-positive bacteria and some Gram-negative bacteria. Sulfonamides exert their antibacterial effects by competing with PABA for dihydrofolate synthetase, hindering the synthesis of folate in sensitive bacteria. Sulfonamides have no effect on already synthesized folic acid, so the effect occurs slowly. Bacteria that can utilize exogenous folic acid are not sensitive to sulfonamides. Livestock and poultry cells can directly utilize folic acid, so they are not easily affected by sulfonamides blocking folic acid synthesis.

It has high antibacterial activity against common aerobic Gram-positive bacteria, such as Staphylococcus aureus (including those resistant to penicillin G), Staphylococcus epidermidis, beta-hemolytic Streptococcus, viridans Streptococcus and Streptococcus pneumoniae. It has good antibacterial effect on anaerobic bacteria, including Clostridium diphtheriae, and Clostridium perfringens. It has no activity against Gram-negative bacteria such as Enterococcus, meningococci, Neisseria gonorrhoeae, and Haemophilus influenzae, as well as fungi. There is no cross-resistance with penicillin, chloramphenicol, cephalosporins and tetracyclines, and there is partial cross-resistance with macrolides. It acts on the 50S subunit of the ribosome of sensitive bacteria, preventing the extension of the peptide chain, thereby inhibiting the protein synthesis of bacterial cells. It is generally an antibacterial agent, but at high concentrations, it also has a bactericidal effect on certain bacteria.

This product is an amide local anesthetic. After blood absorption or intravenous administration, it has obvious biphasic effects of excitation and inhibition on the central nervous system, and there may be no precursor excitation. When the blood concentration is low, analgesia and drowsiness occur, and the pain threshold increases; with increasing doses, the effect or toxicity increases, and it has an anticonvulsant effect at sub-toxic blood concentrations; convulsions may occur when the blood concentration exceeds 5μg·ml-1. At low doses, this product can promote the outflow of K in myocardial cells, reduce myocardial autonomy, and have an anti-ventricular arrhythmia effect; at therapeutic doses, it has no obvious effect on the electrical activity of myocardial cells, atrioventricular conduction, and myocardial contraction; further increases in blood concentrations can cause a slowing of heart conduction velocity, atrioventricular conduction block, inhibition of myocardial contractility, and a decrease in cardiac output.

It has a peripheral anti-M cholinergic receptor effect, can relieve smooth muscle spasms caused by acetylcholine, can also relieve microvascular spasms, and improve microcirculation. It has a relaxing effect on gastrointestinal smooth muscle and inhibits its peristalsis. Its effect is slightly weaker than atropine, and its effect of inhibiting digestive gland secretion is 1/10 of atropine. Its effect of inhibiting salivary gland secretion and dilating pupils is weaker, which is 1/20 to 1/10 of atropine. Because it is not easy to pass through the blood-cerebrospinal fluid barrier, its central effect is also weaker than atropine.

It has a peripheral anti-M cholinergic receptor effect, can relieve smooth muscle spasms caused by acetylcholine, can also relieve microvascular spasms, improve microcirculation, relax gastrointestinal smooth muscle, and inhibit its peristalsis. Its effect is slightly weaker than atropine, and its effect of inhibiting digestive gland secretion is 1/10 of atropine. Its effect of inhibiting saliva secretion and dilating pupils is weaker, which is 1/20-1/10 of atropine. Because it is not easy to pass through the blood-cerebrospinal fluid barrier, its central effect is also weaker than atropine.