Reversible inhibition of rapid axonal transport in vivo by lidocaine hydrochloride.

Rats were given standardized injections of 3H-L-proline into the trigeminal ganglion and 14C-lidocaine hydrochloride at the infraorbital foramen. The 3H-L-proline was always injected 2.5 h before removal of the nerve. Lidocaine, 1, 2, and 4%, produced a concentration-related inhibition of entry of 3H-labeled rapid axonal transport into the distal portions of the nerve. Addition of epinephrine, 1:200,000, doubled the intensity of the effect. The time delay of recovery was also concentration-related, and with 4% lidocaine recovery still seemed incomplete after 4.5. h. It is concluded that inhibition of rapid axonal transport is probably a usual byproduct of nerve block with local anesthetics such as lidocaine. The inhibition seems attributable in part to a disturbance of the energy metabolism of the nerve.