Nitrous Oxide Effects on Cerebral Evoked Potential to Pain

Abstract

The effect of naloxone, 0.4 mg, on the analgesia induced by nitrous oxide, 33%, in O2 was studied in 12 volunteers. Studies in animals suggested that endogenous opiate-like substances may play a major role in the analgesic mechanism of nitrous oxide, but the issue had not been studied in man. Cerebral evoked potentials (CEP) to painful toothpulp electrical shocks were obtained before and after inhalation of nitrous oxide, and after nitrous oxide plus naloxone, 0.4 mg, in 1 session; and before and after inhalation of room air and after room air plus naloxone, 0.4 mg, in another session. CEP waveforms seen between 80-350 ms were quantified in terms of 3 peak-to-peak amplitudes and peak latencies. Nitrous oxide decreased each of the waveform peak-to-peak amplitudes 48%. Naloxone restored the peak-to-peak amplitude of the negative-going wave occurring between 100-175 ms. Nitrous oxide increased the negative peak latency at 175 ms, and naloxone restored this peak latency to normal levels. Neither room air nor room air plus naloxone altered CEP amplitudes or latencies. Over time a significant trend in subjective reports of decreased pain intensity with nitrous oxide and partially increased pain with naloxone was evident. Apparently some effects of nitrous oxide on the CNS can be reversed by naloxone.