In this study the effects of γ-hydroxybutyrate/fentanyl on cerebral blood flow velocity (CBFV) (as measured in the middle cerebral artery by transcranial Doppler ultrasonography) and on cerebrovascular carbon dioxide reactivity were investigated. Mean CBFV (̇Vmean) and haemodynamic responses were recorded in 12 non-neurosurgical patients before, during and after induction of general anaesthesia with γ-hydroxybutyrate (GHB) (20 min constant rate infusion of 100 mg kg−1). Two patients were excluded, one because of bradycardia and the other because of severe myoclonia. During the infusion of GHB, normocapnia was maintained by manually assisting ventilation as necessary. The infusion of GHB did not affect ̇Vmean [awake: 57±12 cm s−1 (mean±SD); 22.5 min: 62±15 cm s−1, NS difference] or mean arterial blood pressure (MAP) (awake: 97±12 mmHg; 22.5 min: 89±10 mmHg, NS). This suggests that cerebral blood flow velocity is unaltered by an anaesthetic dose of GHB. Twenty-five minutes after the start of GHB, fentanyl 3 μg kg−1 and vecuronium 0.1 mg kg−1 were given, the trachea was intubated and the lungs were mechanically ventilated to maintain end-tidal Pco2 of 4.6±0.4 kPa (30 min). At 30 min after the start of the GHB infusion, ̇Vmean and MAP decreased to 38±10 cm s−1 and 76±12 mmHg (both P<0.05 vs 22.5 min) respectively. After adjusting the ventilation to achieve hypocapnia (40 min: end-tidal Pco2 3.5±0.2 mmHg), ̇Vmean decreased to 29±7 cm s−1, while MAP did not change. This allowed the relative vasoreactivity (percentage change in ̇Vmean/0.133 kPa change in the end-tidal Pco2 from normocapnia to hypocapnia) to be estimated as 2.7±1.6% 0.133 kPa−1. This suggests that cerebrovascular response to CO2 during γ-hydroxybutyrate/fentanyl anaesthesia is maintained.
