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.