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Lidocaine Anesthetic Information

Topical Pain Reliever


All lidocaine anesthetic is a membrane stabilizing drugs; they reversibly decrease the rate of depolarization and repolarization of excitable membranes (like nociceptors). Though many other drugs also have membrane stabilizing properties, all are not used as local anesthetics, for example propranolol. Lidocaine anesthetic drugs act mainly by inhibiting sodium influx through sodium-specific ion channels in the neuronal cell membrane, in particular the so-called voltage-gated sodium channels. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Lidocaine anesthetic drugs bind more readily to sodium channels in activated state, thus onset of neuronal blockade is faster in neurons that are rapidly firing. This is referred to as state dependent blockade.


Lidocaine anesthetics are weak bases and are usually formulated as the hydrochloride salt to render them water-soluble. At the chemical’s pKa the protonated (ionised) and unprotonated (unionized) forms of the molecule exist in equilibrium but only the unprotonated molecule diffuses readily across cell membranes. Once inside the cell the lidocaine anesthetic will be in equilibrium, with the formation of the protonated (ionised form), which does not readily pass back out of the cell. This is referred to as “ion-trapping”. In the protonated form, the molecule binds to the local anesthetic binding site on the inside of the ion channel near the cytoplasmic end.


Acidosis such as caused by inflammation at a wound partly reduces the action of lidocaine anesthetics. This is partly because most of the lidocaine anesthetic is ionized and therefore unable to cross the cell membrane to reach its cytoplasmic-facing site of action on the sodium channel.


All nerve fibers are sensitive to lidocaine anesthetics, but generally, those with a smaller diameter tend to be more sensitive than larger fibers. Lidocaine anesthetics block conduction in the following order: small myelinated axons (e.g. those carrying nociceptive impulses), non-myelinated axons, and then large myelinated axons. Thus, a differential block can be achieved (i.e. pain sensation is blocked more readily than other sensory modalities).


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