Chemical Properties
White to Off-White Solid
Originator
Xylocaine,Astra,US,1949
Uses
Anesthetic (local); antiarrhythmic (class IB). Long-acting, membrane stabilizing agent against ventricular arrhythmia. Originally developed as a local anesthetic.
Uses
Apply to affected site 5 to 10 minutes before procedure. Duration of
anesthesia is relatively short (<1 hour).
Uses
Local anesthesic;Na+ channel blocker
Definition
ChEBI: The anhydrous form of the hydrochloride salt of lidocaine.
Manufacturing Process
One mol of 2,6-xylidine is dissolved in 800 ml glacial acetic acid. The mixture
is cooled to 10°C, after which 1.1 mol chloracetyl chloride is added at one
time. The mixture is stirred vigorously during a few moments after which
1,000 ml half-saturated sodium acetate solution, or other buffering or
alkalizing substance, is added at one time. The reaction mixture is shaken
during half an hour. The precipitate formed which consists of ω-chloro-2,6-
dimethyl-acetanilide is filtered off, washed with water and dried. The product
is sufficiently pure for further treatment. The yield amounts to 70 to 80% of
the theoretical amount.
One mole of the chloracetyl xylidide thus prepared and 2.5 to 3 mols diethyl
amine are dissolved in 1,000 ml dry benzene. The mixture is refluxed for 4 to
5 hours. The separated diethyl amine hydrochloride is filtered off. The benzene
solution is shaken out two times with 3N hydrochloric acid, the first time with
800 ml and the second time with 400 ml acid. To the combined acid extracts
is added an approximately 30% solution of sodium hydroxide until the
precipitate does not increase.
The precipitate, which sometimes is an oil, is taken up in ether. The ether
solution is dried with anhydrous potassium carbonate after which the ether is
driven off. The remaining crude substance is purified by vacuum distillation.
During the distillation practically the entire quantity of the substance is carried
over within a temperature interval of 1° to 2°C. The yield approaches the
theoretical amount. MP 68° to 69°C. BP 180° to 182°C at 4 mm Hg; 159° to
160°C at 2 mm Hg. (Procedure is from US Patent 2,441,498.)
Brand name
Alpha caine Hydrochloride (Carlisle); Anestacon (Polymedica);
Laryng-O-Jet (International Medication); Lidocaton (Phar maton); Lidopen (Meridian); Xylocaine (Abraxis); Xylo caine (AstraZeneca); Xylocaine (Dentsply).
Therapeutic Function
Local anesthetic, Antiarrhythmic
Biological Functions
Lidocaine hydrochloride (Xylocaine) is the most commonly
used local anesthetic. It is well tolerated, and in
addition to its use in infiltration and regional nerve
blocks, it is commonly used for spinal and topical anesthesia
and as an antiarrhythmic agent.
Lidocaine has a more rapidly occurring, more intense,
and more prolonged duration of action than does procaine.
General Description
Lidocaine hydrochloride,2-(diethylamino)-2 ,6 -acetoxylidide monohydrochloride(Xylocaine), was conceived as a derivative of gramine(3-dimethylaminomethylindole) and introduced as a localanesthetic. It is now being used intravenously as a standardparenteral agent for suppression of arrhythmias associatedwith acute myocardial infarction and cardiac surgery.It isthe drug of choice for the parenteral treatment of prematureventricular contractions.
Mechanism of action
Lidocaine can block Na+ and K+ ion channels and regulate intracellular and extracellular calcium concentrations through other ligand-gated ion channels. Lidocaine was the first sodium channel blocker to be identified. Its main mechanism of action is blocking voltage-gated Na+ channels (VGSC/NaVs).
Clinical Use
Lidocaine hydrochloride is a class IB antiarrhythmicagent with a different effect on the electrophysiologicalproperties of myocardial cells from that of procainamideand quinidine. It binds with equal affinity to the active (A)and inactive (I) Na+ ion channels. It depresses diastolic depolarizationand automaticity in the Purkinje fiber networkand increases the functional refractory period relative toaction potential duration, as do procainamide and quinidine.It differs from the latter two drugs, however, in that it doesnot decrease, and may even enhance, conduction velocity and increase membrane responsiveness to stimulation.There are fewer data available on the subcellular mechanismsresponsible for the antiarrhythmic actions of lidocainethan on the more established drug quinidine. It has been proposedthat lidocaine has little effect on membrane cation exchangeof the atria. Sodium ion entrance into ventricularcells during excitation is not influenced by lidocaine becauseit does not alter conduction velocity in this area.Lidocaine hydrochloride does depress Na+ influx duringdiastole, as do all other antiarrhythmic drugs, to diminishautomaticity in myocardial tissue. It also alters membraneresponsiveness in Purkinje fibers, allowing increased conductionvelocity and ample membrane potential at the timeof excitation.
storage
Store in a tightly closed container at room temperature away from light
and moisture. Do not store in the bathroom. Do not freeze. Keep all medications away from children and pets.
