It has a significant effect of increasing the number of peripheral blood leukocytes in normal rabbits. The peak value of leukocyte count occurs on the 4th day after the first administration, which is 72% higher than that before administration, which is better than the leukocyte-increasing drug shark liver alcohol. It has a significant effect of increasing leukocytes in rabbits induced by cobalt 60-gamma ray and deep X-ray irradiation. It also has a preventive effect on leukocyte decrease when administered two days before irradiation. It can prevent leukopenia in mice caused by mitomycin C. It has a synergistic inhibitory effect on the solid type of Ehrlich carcinoma when used in combination with cyclophosphamide, and the toxicity of leukocyte decrease caused by cyclophosphamide is significantly reduced.

It has high antibacterial activity against common aerobic Gram-positive bacteria, such as Staphylococcus aureus (including those resistant to penicillin G), Staphylococcus epidermidis, β-hemolytic Streptococcus, viridans Streptococcus and Streptococcus pneumoniae. It has good antibacterial effect against anaerobic bacteria, including Clostridium tetani, Corynebacterium 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, which has a biphasic effect of excitation and inhibition on the central nervous system; at low doses, analgesia and drowsiness occur, and the pain threshold is increased; when the dose is increased, the effect or toxicity is enhanced, and at sub-toxic blood concentrations, there is an anticonvulsant effect; convulsions may occur when the blood concentration is too high. At low doses, it 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 significant effect on myocardial cell electrical activity, atrioventricular conduction, and myocardial contraction; when the blood concentration is increased, it can slow down the heart conduction velocity, cause atrioventricular conduction block, inhibit myocardial contractility, and reduce cardiac output.

Restores the imbalance between the excitation and inhibition processes of the cerebral cortex, and has central inhibitory effects such as sedation, hypnosis and analgesia

Nimodipine is a Ca2 channel blocker that inhibits smooth muscle contraction and relieves vasospasm by preventing Ca2 from entering cells. It has a strong effect on cerebral arteries and can pass through the blood-brain barrier to prevent vasospasm after subarachnoid hemorrhage, protect and promote memory, promote intellectual recovery, dilate cerebral blood vessels, increase cerebral blood flow, and reduce ischemic brain damage.