Background and Objectives Although meperidine safely produces clinical spinal anesthesia, the responsible mechanism is unknown. This study was undertaken to test the possibility that this drug acts as a local anesthetic by investigating its ability to inhibit conduction in a human peripheral nerve.
Methods In a blinded fashion, the abilities of 5-mL injections of meperidine (0.5% and 1.5%), lidocaine (0.25%), and saline to produce median nerve block were tested in eight volunteer subjects, and these four solutions were compared with standard local anesthetic solutions that had been tested in previous studies. The extent of local anesthesia was measured objectively by eletrodiagnostic tests, namely, compound motor action potentials (CMAPs) and sensory nerve action potentials (SNAPs), as well as by qualitative tests of sensation.
Results Lidocaine (0.25%) prolonged median SNAP latency from 3.1 ms to 3.3 ms (P < .015) and prolonged mean CMAP latency from 4.1 ms to 4.7 ms (P < .002). The SNAP amplitude trended downward after lidocaine (0.25%), but the decrease did not reach statistical significance (35 μV to 25 μV, P < .19). Neither meperidine solution (0.5% or 1.5%) nor saline inhibited SNAP or CMAP amplitudes or prolonged SNAP or CMAP latencies. Also, in contrast to previous findings with more potent local anesthetic solutions (eg, lidocaine 1%, mepivacaine 1%, and bupivacaine 0.33%), none of the four solutions tested in this study altered subjective sensations of hot, cold, or pinprick. Meperidine 1.5% produced systemic side effects, including vertigo, nausea, and flushing, in all subjects.
Conclusions Meperidine produced no signs of local anesthesia, even when given at a dose (75 mg) and concentration (1.5%) that consistently produced systemic side effects. Thus, the coequivalent ability of meperidine and lidocaine to produce spinal anesthesia contrasts with their discordant ability to produce local anesthesia. This disparity suggests that meperidine may produce spinal anesthesia through mechanisms other than inhibition of sodium channel function.
- local anesthetics
- impulse conduction
- median nerve
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Presented in part at the meeting of the American Society of Anesthesiologists, October 1993, Washington, D.C.
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