• P Amorim, G Chambers, J Cottrell, and I S Kass.
• Department of Anesthesiology, State University of New York, Health Science Center at Brooklyn, 11203, USA.
• Anesthesiology. 1997 Sep 1;87(3):642-51.

BackgroundResearch has suggested that nitrous oxide may be harmful to ischemic neurons; however, the evidence for this is equivocal. The authors used rat hippocampal slices to examine the effects of nitrous oxide on neuronal hypoxic damage.MethodsThe evoked population spike (PS) was recorded from hippocampal CA1 pyramidal cells before, during, and after hypoxia. Control groups received nitrogen concentrations equal to nitrous oxide throughout the experiments. Biochemical measurements were made from dissected CA1 regions under experimental conditions that matched the electrophysiology studies.ResultsRecovery of the PS after hypoxia was 18 +/- 7% in slices treated with 50% nitrous oxide before and during 3.5 min of hypoxia; this compares with 41 +/- 9% (P < 0.05) in nitrogen-treated slices. Slices treated with nitrous oxide (95%) only during hypoxia (6 min) also demonstrated significantly less recovery of the PS than did slices treated with nitrogen. There was no significant difference in recovery if nitrous oxide was discontinued after the hypoxic period. Adenosine triphosphate concentrations after 3.5 min of hypoxia in slices treated with nitrous oxide decreased to the same extent as in nitrogen-treated slices (47% vs. 50%). Calcium influx increased during 10 min of hypoxia in untreated slices, but nitrous oxide did not significantly increase calcium influx during hypoxia. The sodium concentrations increased and potassium concentrations decreased during hypoxia; nitrous oxide did not significantly alter these changes.ConclusionsNitrous oxide impaired electrophysiologic recovery of hippocampal slices after severe hypoxia. Nitrous oxide did not cause significant changes in the biochemical parameters examined.

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