Failure of naloxone to reverse the nitrous oxide-induced depression of a brain stem reflex: an electrophysiologic and double-blind study in humans.
The effects of 33% nitrous oxide on the two components of the blink reflex were studied on seven healthy volunteers. The blink responses were elicited by a supraorbital nerve stimulation and recorded from the ipsilateral orbicularis oculi muscle. The intensity of stimulation was chosen at two to three times the reflex threshold in order to obtain stable suprathreshold reflex responses as well as a tolerable pain sensation reported by the volunteers. Nitrous oxide administration resulted in a potent depression of the two components of the blink reflex. This depressive effect was more marked upon the late (R2) nociceptive component (83%) than upon the early (R1) component (41%). Simultaneously, subjects reported either a decrease in pain sensation or an indifference toward the painful stimulus. None of these effects were reversed by a double-blind intravenous naloxone (1.4 mg) injection. The analgesic effect of nitrous oxide is a nonspecific depressant action on the transmission of the nociceptive messages in central nervous structures, independent of pain-suppressive endogenous morphine-like systems.
D000328:Adult; D001767:Blinking / Q000187:drug effects*; D001933:Brain Stem / Q000187:drug effects / Q000502:physiology*; D003864:Depression, Chemical; D004311:Double-Blind Method; D004576:Electromyography; D005260:Female; D006801:Humans; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009609:Nitrous Oxide / Q000494:pharmacology*
D009270:Naloxone; D009609:Nitrous Oxide