Cerebral Effects of Nitrous Oxide in the Dog

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Abstract
Cerebral effects of NO, 60%, were examined in 27 dogs. During administration of halothane, 0.2%, NO increased cerebral blood flow (CBF) and cerebral metabolic rate for xoygen (CMRO2) to a maximum of 203 and 121% of control, respectively. CSF pressure paralleled the change in CBF. The EEG showed low-voltage slow-wave activity. With halothane, 0.8% NO increased CBF and CMRO2 to maximum values of 164 and 108% of control, respectively. After administration of thiamylal, 8 mg/kg, i.v., NO did not increase CBF or CMRO2 for the first 3C-min period, but thereafter, CMRO2 increased to 11% above control. Pretreatment with reserpine, 0.5 mg/kg, i.m. for 2 days did not modify cerebral circulatory and metabolic responses to NO. NO may cause 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 CMRO2. Cerebral effects of NO are modified by the background anesthesia.

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