Cerebral Effects of Nitrous Oxide

The cerebral effects of 60 per cent (end-tidal concentration) nitrous oxide (N_2O) were examined in 29 dogs. With the inhalation of N_2O, the cerebral blood flow (CBF) increased, reaching a peak of 203 per cent of the control value at 7 minutes, and thereafter decreased gradually to 125 per cent of the control over a 60 minute-period. The mean cerebral metabolic rate for oxygen (CMR_O2) increased to about 120 per cent of the control value within 15 minutes and remained elevated during the inhalation of N_2O. There was no significant change in the mean arterial pressure (MAP), but a significant reduction in cerebral vascular resistance (CVR) was observed. The electroencephalogram (EEG) showed low voltage, slow wave activity with the inhalation of N20. After the intravenous injection of thiamyla1 (8 mg/kg), N_2O increased neither the CBF nor CMR_O2 for the first 30 minute-period, but produced predominant slow wave activity during the period. Pretreatment with reserpine (total 1.0 mg/kg) did not modify significantly the cerebral circulatory, metabolic and electrographic effects of N_2O. The cerebral responses to the alteration in Paco_2 did not differ significantly during increased metabolism with N_2O from the control without N_2O. In conclusion, N_2O is a cerebral metabolic stimulant which accompanies the increase in the CBF, and EEG slowing. The cerebral circulatory and metabolic stimulation was blocked by prior administration of thiamylal but not by pretreatment with reserpine.