Local Anesthetic Pharmaceutical Intermediates 99% Lidocaine Hydrochloride Lidocaine HCl

CAS: 137-58-6
Assay: 99%
MF: C14H23N2O58
MW: 235.3447
Reference Standard: BP2002/USP28
Character: White crystalline powder
Usage: It replaces procaine,being widely used in plastic and cosmetic operation in local infiltration anesthesia, the sodium channel inhibition of the nerve cell membrane to block nerve excitability and conduction.

Description:

Mechanism of action: Lidocaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action.

Hemodynamics: Excessive blood levels may cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. With central neural blockade these changes may be attributable to block of autonomic fibers, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system and/or the beta-adrenergic receptor stimulating action of epinephrine when present. The net effect is normally a modest hypotension when the recommended dosages are not exceeded.

Applications:

Lidocaine crosses the blood-brain and placental barriers, presumably by passive diffusion.

Lidocaine is metabolized rapidly by the liver, and metabolites and unchanged drug are excreted by the kidneys. Biotransformation includes oxidative N-dealkylation, ring hydroxylation, cleavage of the amide linkage, and conjugation. N-dealkylation, a major pathway of biotransformation, yields the metabolites monoethylglycinexylidide and glycinexylidide. The pharmacological/toxicological actions of these metabolites are similar to, but less potent than, those of Lidocaine. Approximately 90% of Lidocaine administered is excreted in the form of various metabolites, and less than 10% is excreted unchanged. The primary metabolite in urine is a conjugate of 4-hydroxy-2, 6-dimethylaniline.

Local Anesthetic Pharmaceutical Intermediates 99% Lidocaine Hydrochloride Lidocaine HCl

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