Pharmaceutical Intermediates 99% Lidocaine Hydrochloride Lidocaine
HCl for Local Anesthetic
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.
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.
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,
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