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ANESTHETIC PHARMACOLOGY

Nitrous Oxide-Induced Analgesia Does Not Influence Nitrous Oxide's Immobilizing Requirements

Steven L. Jinks, PhD^*, Earl Carstens, PhD, and Joseph F. Antognini, MD^*

From the Departments of *Anesthesiology and Pain Medicine, and Neurobiology, Physiology and Behavior, University of California, Davis, Davis, California 95616.

Address correspondence and reprint requests to Steven L. Jinks, PhD, Department of Anesthesiology and Pain Medicine, TB-170, University of California School of Medicine, Davis, CA 95616. Address e-mail to sljinks{at}ucdavis.edu.

BACKGROUND: Nitrous oxide (N₂O) acts on supraspinal noradrenergic neurons to produce analgesia, but it is unclear if analgesia contributes to N₂O's immobilizing effects. We tested the hypothesis that N₂O minimum alveolar anesthetic concentration (MAC) is unchanged after selective ablation of supraspinal noradrenergic neurons, or in naïve animals at N₂O exposure timepoints when analgesia is absent.

METHODS: We determined tailflick latency (TFL) and hindpaw withdrawal latency (HPL) under 70% N₂O, N₂O MAC, and isoflurane MAC before and after intracerebroventricular injections of anti-dopamine-β hydroxylase conjugated to saporin (SAP-DBH; n = 7), or a control antibody conjugated to saporin (n = 5). In a separate group of naive rats (n = 8), N₂O MAC was determined at 25–45 min after initiation of N₂O exposure (during peak analgesia) and again at 120–140 min (after TFL and HPL returned to baseline).

RESULTS: After 30 min of N₂O exposure, TFL and HPL increased significantly but declined back to baseline within 120 min. N₂O did not produce analgesia in rats that received SAP-DBH. However, N₂O and isoflurane MAC were not significantly different between SAP-DBH and control-injected animals (Mean ± sd for N₂O: 1.7 ± 0.1 atm vs 1.7 ± 0.2 atm; isofurane: 1.6 ± 0.2% vs 1.7 ± 0.2%). In naïve animals, N₂O MAC was not different at the 30 min period compared with the 120 min period (1.8 ± 0.1 atm vs 1.8 ± 0.2 atm).

CONCLUSIONS: Destroying brainstem noradrenergic neurons or prolonged exposure to N₂O removes its analgesic effects, but does not change MAC. The immobilizing mechanism of N₂O is independent from its analgesic effects.