Animal studies have shown that dihydroergoline mesylate changes brain neurotransmission, and data show that it has an excitatory effect on dopamine and 5-hydroxytryptamine receptors and a blocking effect on alpha-adrenergic receptors. It improves impaired brain metabolic function and shortens brain circulation time, an effect reflected in changes in brain electrical activity, with significant changes in the power spectrum of the electroencephalogram (EEG).

Animal studies have shown that dihydroergoline mesylate changes brain neurotransmission, and data show that it has an excitatory effect on dopamine and 5-hydroxytryptamine receptors and a blocking effect on alpha-adrenergic receptors. It improves impaired brain metabolic function and shortens brain circulation time, an effect reflected in changes in brain electrical activity, with significant changes in the power spectrum of the electroencephalogram (EEG).

Animal studies have shown that dihydroergoline mesylate changes brain neurotransmission, and data show that it has an excitatory effect on dopamine and 5-hydroxytryptamine receptors and a blocking effect on alpha-adrenergic receptors. It improves impaired brain metabolic function and shortens brain circulation time, an effect reflected in changes in brain electrical activity, with significant changes in the power spectrum of the electroencephalogram (EEG).

It changes the neurotransmission in the brain, has an excitatory effect on dopamine and 5-hydroxytryptamine receptors, a blocking effect on alpha-adrenaline receptors, improves damaged brain metabolic function, and shortens cerebral circulation time. This effect is reflected in changes in the electrical activity of the brain, with significant changes in the power spectrum of the electroencephalogram (EEG).

It changes the neurotransmission in the brain, has an excitatory effect on dopamine and 5-hydroxytryptamine receptors, a blocking effect on alpha-adrenaline receptors, improves damaged brain metabolic function, and shortens cerebral circulation time. This effect is reflected in changes in the electrical activity of the brain, with significant changes in the power spectrum of the electroencephalogram (EEG).

Cefixime is a third-generation oral cephalosporin that kills bacteria by inhibiting bacterial cell wall synthesis. It is stable to most β-lactamases, and many strains producing penicillinase and cephalosporinase are still sensitive to this product. Cefixime has good antibacterial effects in vitro and in vivo against Gram-positive cocci such as pneumococci, Streptococcus pyogenes, and Gram-negative bacilli such as Haemophilus influenzae (including enzyme-producing strains), Moraxella catarrhalis (including enzyme-producing strains), Escherichia coli, Proteus mirabilis, and Neisseria gonorrhoeae (including enzyme-producing strains). Cefixime also has antibacterial activity against Streptococcus pneumoniae, Parainfluenzae, Proteus vulgaris, Klebsiella pneumoniae, Pasteurella multocida, Providencia, Salmonella, Shigella, Serratia marcescens, Citrobacter heteromorphis, and Citrobacter malonate, but its clinical effectiveness has not yet been established. This product has poor antibacterial effect on Staphylococcus, and has no antibacterial effect on Pseudomonas aeruginosa, Enterobacter, Bacteroides fragilis, Clostridium, etc.

The third generation of oral cephalosporins kills bacteria by inhibiting bacterial cell wall synthesis. It is stable to most β-lactamases, and many strains producing penicillinase and cephalosporinase are still sensitive to this product. It has good antibacterial effects on Gram-positive cocci such as pneumococci, Streptococcus pyogenes, and Gram-negative bacilli such as Haemophilus influenzae (including enzyme-producing strains), Moraxella catarrhalis (including enzyme-producing strains), Escherichia coli, Proteus mirabilis, and Neisseria gonorrhoeae (including enzyme-producing strains). It also has antibacterial activity in vitro against Streptococcus pneumoniae, Parainfluenzae, Proteus vulgaris, Klebsiella pneumoniae, Pasteurella multocida, Providencia, Salmonella, Shigella, Serratia marcescens, Citrobacter heteromorphis, and Citrobacter malonate, but its clinical effectiveness has not yet been established. It has poor antibacterial effects on Staphylococcus, and has no antibacterial effects on Pseudomonas aeruginosa, Enterobacter, Bacteroides fragilis, Clostridium, etc.

The third generation of oral cephalosporins kill bacteria by inhibiting bacterial cell wall synthesis. They are stable to most β-lactamases and have good antibacterial effects on Gram-positive cocci such as pneumococci and Streptococcus pyogenes, and Gram-negative bacilli such as Haemophilus influenzae (including enzyme-producing strains), Moraxella catarrhalis (including enzyme-producing strains), Escherichia coli, Proteus mirabilis, and Neisseria gonorrhoeae (including enzyme-producing strains). In vitro, they also have antibacterial activity against Streptococcus pneumoniae, Parainfluenzae, Proteus vulgaris, Klebsiella pneumoniae, Pasteurella multocida, Providencia, Salmonella, Shigella, Serratia marcescens, Citrobacter heteromorphis, and Citrobacter malonate, but their clinical effectiveness has not yet been established. They have poor antibacterial effects on Staphylococcus, and have no antibacterial effects on Pseudomonas aeruginosa, Enterobacter, Bacteroides fragilis, and Clostridium.