NITROUS-OXIDE INCREASES CEREBRAL BLOOD-FLOW VELOCITY DURING PHARMACOLOGICALLY INDUCED EEG SILENCE IN HUMANS

We examined the effect of nitrous oxide on cerebral blood flow velocit y (Vmca), arteriovenous oxygen content difference and cerebral use of glucose during propofol-induced electrical silence of the electroencep halogram (EEG) in 10 patients undergoing anesthesia for nonneurosurgic al procedures. Anesthesia was induced with propofol 2.5 mg/kg, fentany 3 mug/kg (followed by an infusion of 2 mug/kg/h), vecuronium 0.1 mg/k g, and maintained with a propofol infusion (250-300 mug/kg/min) suffic ient to induce EEG silence. A transcranial Doppler was used to measure the Vmca and a jugular bulb catheter was inserted for oxygen saturati on and glucose use measurements. After a 15-period of isoelectric EEG and normocapnia (P(a)CO2 38 +/- mm Hg), baseline arterial and jugular bulb venous blood gases were drawn, and mean arterial pressure (MAP), heart rate (HR), and Vmca were recorded. Nitrous oxide was then introd uced and equilibrated to an end-tidal concentration of 70% for 15 min, after which MAP, HR, Vmca, arterial and jugular bulb venous blood gas es were measured again. Nitrous oxide increased Vmca (29 +/- 4 to 35 /- 4 cm/s, p < 0.01), cerebral use of oxygen (166 +/- 13 to 190 +/- 12 vol%-cm/s, p < 0.05) and glucose (245 +/- 38 to 290 +/- 48 g%-cm/s, p < 0.05) by approximately 20%. Occasional bursts of EEG activity were observed in eight patients studied during the N2O stage. We conclude t hat in patients with propofol-induced isoelectric EEG, the increase se en in Vmca with the introduction of N2O is mainly due to cerebral stim ulation and increase in cerebral metabolic rate.