The effects of PaCO₂ on the cerebrovascular response to nitrous oxide in the halothane-anesthetized rabbit

Several authors have observed that nitrous oxide increases cerebral blood flow (CBF) and/or intracranial pressure (ICP) in experimental situations and in humans. However, the effects of hypocapnia on the cerebrovascular responses to N₂O have not been investigated. Therefore, six New Zealand White rabbits were anesthetized with ~1.0 MAC halothane (mean end-tidal concentration 1.26%) and surgically prepared for recording of ICP, the EEG, and both cortical and global CBF (by the H₂-clearance method). After preparation was complete, measurements were obtained during ventilation with 70% nitrogen (in O₂), and after the inspired gas mixture was changed to 70% N₂O (still with 1.0 MAC halothane). Two such data pairs (N₂-N₂O) were obtained, one during hypocarbia (PaCO₂ ~ 20 mm Hg) and the other during normocarbic (PaCO₂ ~ 40 mm Hg) conditions. Mean arterial pressure (MABP) was held constant within each data pair by infusing angiotensin II as needed. Nitrous oxide resulted in a consistent increase in EEG frequency and decrease in amplitude as compared with N₂, and produced small (~ 1 mm Hg) but statistically significant increases in ICP during both hypo- and normocarbic conditions. Nitrous oxide administration also increased CBF as measured both in frontal cortex and globally, with similar changes seen during hypo- and normocarbic conditions, e.g., cortical CBF increased from 42 ± 8 to 59 ± 15 ml·100 gm^-1·min^-1 during hypocarbia, and from 61 ± 13 to 75 ± 15 ml·100gm^-1·min^-1 during normocarbia. These results confirm that N₂O is a potent cerebrovasodilator in the rabbit, and also indicate that reductions in PaCO₂ do not blunt the cerebrovascular responses to N₂O.