CEREBRAL EFFECTS OF NITROUS-OXIDE IN DOG

The cerebral effects of nitrous oxide, 60%, were examined in 27 dogs. During administration of halothane, 0.2%, nitrous oxide increased cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMR(O)2) to a maximum of 203 and 121% of control, respectively. Cerebrospinal fluid pressure paralleled the change in CBF. The electroencephalogram (EEG) showed low-voltage slow-wave activity. With halothane, 0.8%, nitrous oxide increased CBF and CMR(O)2 to maximum values of 164 and 108% of control, respectively. After administration of thiamylal, 8 mg/kg, intravenously, nitrous oxide did not increase CBF or CMR(O)2 for the first 30 min period, but thereafter, CMR(O)2 increased to 11% above control. Pretreatment with reserpine, 0.5 mg/kg, intramuscularly, for two days did not modify the cerebral circulatory and metabolic responses to nitrous oxide. These results indicate that nitrous oxide causes cerebral metabolic stimulation accompanied by an increase in CBF and slowing of the EEG. Sympathoadrenal stimulation would appear not to be the mechanism for the increases in CBF and CMR(O)2. The cerebral effects of nitrous oxide are modified by the background anesthesia.