NITROUS-OXIDE IMPAIRS ELECTROPHYSIOLOGIC RECOVERY AFTER SEVERE HYPOXIA IN RAT HIPPOCAMPAL SLICES

Background Research has suggested that nitrous oxide may be harmful to ischemic neurons; however, the evidence for this is equivocal. The au thors used rat hippocampal slices to examine the effects of nitrous ox ide on neuronal hypoxic damage. Methods: The evoked population spike C PS) was recorded from hippocampal CA1 pyramidal cells before, during, and after hypoxia. Control groups received nitrogen concentrations equ al to nitrous oxide throughout the experiments. Biochemical measuremen ts were made from dissected CA1 regions under experimental conditions that matched the electrophysiology studies. Results: Recovery of the P S 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 les s recovery of the PS than did slices treated with nitrogen. There was no significant difference in recovery if nitrous oxide was discontinue d after the hypoxic period. Adenosine triphosphate concentrations afte r 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 nit rous oxide did not significantly increase calcium influx during hypoxi a. The sodium concentrations increased and potassium concentrations de creased during hypoxia; nitrous oxide did not significantly alter thes e changes. Conclusions: Nitrous oxide impaired electrophysiologic reco very of hippocampal slices after severe hypoxia. Nitrous oxide did not cause significant changes in the biochemical parameters examined.