The Effect of Nitrous Oxide on Canine Cerebral Metabolism

Cerebral blood flow and arterial–sagittal differences for oxygen have been measured in unpremedicated dogs maintained at, 37.0 C. All were paralyzed, had received a spinal anesthetic, and were artificially ventilated. In each of a first group, measurements with and without halothane were carried out with 70 per cent N2O in O2 and with 70 per cent N2 in O2. In a second group, either N2O or N2 was used throughout and measurements were made in the absence of halothane and at 0.1, 0.4, and 0.7 per cent halothane (alveolar). In the absence of halothane and at 0.1 per cent halothane, the average rate of consumption of O2 by the brain (CMRo2) was 11 per cent greater with N2O than with N2. At 0.4 and 0.7 per cent halothane, CMRo2 was greater with N2O but the differences were not significant. It is concluded that N2O per se is not a cerebral metabolic depressant and that the anesthetic action of N2O is not based on generalized cerebral metabolic depression.