Voltage-gated sodium channels (VGSC, Na_V) are critically important for electrogenesis and nerve impulse conduction. Certain sodium channel isoforms are predominantly expressed in peripheral sensory neurons associated with pain sensation, and the expression and functional properties of Na_V in peripheral sensory neurons can be dynamically regulated following axonal injury or peripheral inflammation¹.

Lorcainide is an acetanilide derivative which blocks Na_V channels. It possesses both local anesthetic and antiarrhythmic^2,3 properties and in experimental animals it elevates the ventricular fibrillation threshold and protects against ouabain-induced arrhythmias^4,5. Clinically, it is gaining an important place in the therapy of recurrent premature ventricular contractions⁶, recurrent ventricular tachycardia and repetitive atrial tachycardias^7-9.

Compounds with antiarrhythmic activity show great variation in their chemical structure and have been classified according to: (1) their anatomical site of action; (2) their clinical range of activity; and (3) their electrophysiological action on isolated cardiac fibers. Like other class 1 antiarrhythmic drugs, the primary electrophysiological effect of Lorcainide is the reduction of the rate of rise of action potential during phase 0⁴. Because of the slow recovery kinetics of the sodium ion channel, it has been classified as a class 1 antiarrhythmic agent^10-12.

The effective concentrations for Lorcainide in humans are between 0.2 and 0.5 mg·litre^{-1 13} and 10 μM or 100 μM of Lorcainide may also protect central neuronal axons from hypoxic injury¹⁴.