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Cerebral haemodynamic and electrocortical CO2 reactivity in pigs anaesthetized with fentanyl, nitrous oxide and pancuronium

Cerebral haemodynamic, metabolic and electrocortical reactivity to alterations in arterial CO2, tension (PaCO2) was assessed in seven mechanically ventilated juvenile pigs to test an experimental model designed for cerebral pharmacodynamic and pharmacokinetic studies. The animals were anaesthetized with fentanyl, nitrous oxide and pancuronium and sequentially normo‐ and hyperventilated over a 100‐min period. Five measurements were made at 25‐min intervals. The cerebral blood flow (CBF) was measured with the intraarterial 133Xe technique and the cerebral metabolic rate for oxygen (CMRo2) determined from CBF and the cerebral arteriovenous oxygen content difference. A linear correlation (r = 0.845) was found between CBF and PaCO2. The cerebrovascular reactivity to hypocapnia (ΔCBF/ΔPaCO2) was maintained throughout the experimental period and amounted to (95% confidence interval) 9.1 (7.1–11.1) ml · 100 g‐1 · min‐1 · kPa‐1 within the PaCO2 range 3.3–6.3 kPa. The CMRo2 was not influenced by hyperventilation. The baseline electroencephalographic (EEG) pattern was stable at normocapnia (mean PaCO2 5.6 kPa), whereas spectral values for delta and total average voltage increased significantly (P<0.05) at extensive hypocapnia (3.5 kPa). Maintenance of cerebral CO2 reactivity and spectral EEG voltage at a stable plasma level of fentanyl is complementary to the cerebral haemodynamic and metabolic stability previously found at sustained normocapnia in this model.