Cerebral Blood Volume (CBV) in Humans during Normo- and Hypocapnia: Influence of Nitrous Oxide (N2O)

Background It is generally argued that variations in cerebral blood flow create concomitant changes in the cerebral blood volume (CBV). Because nitrous oxide (N2O) inhalation both increases cerebral blood flow and may increase intracranial pressure, it is reasonable to assume that N2O acts as a general vasodilatator in cerebral vessels both on the arterial and on the venous side. The aim of the current study was to evaluate the effect of N2O on three-dimensional regional and global CBV in humans during normocapnia and hypocapnia. Methods Nine volunteers were studied under each of four conditions: normocapnia, hypocapnia, normocapnia + 40–50% N2O, and hypocapnia + 40–50% N2O. CBV was measured after 99mTc-labeling of blood with radioactive quantitative registration via single photon emission computer-aided tomography scanning. Results Global CBV during normocapnia and inhalation of 50% O2 was 4.25 ± 0.57% of the brain volume (4.17 ± 0.56 ml/100 g, mean ± SD) with no change during inhalation of 40–50% N2O in O2. Decreasing carbon dioxide (CO2) by 1.5 kPa (11 mmHg) without N2O inhalation and by 1.4 kPa (11 mmHg) with N2O inhalation reduced CBV significantly (F = 57, P < 0.0001), by 0.27 ± 0.10% of the brain volume per kilopascal (0.26 ± 0.10 ml · 100 g−1 · kPa−1) without N2O inhalation and by 0.35 ± 0.22% of the brain volume per kilopascal (0.34 ± 0.22 ml · 100 g−1 · kPa−1) during N2O inhalation (no significant difference). The amount of carbon dioxide significantly altered the regional distribution of CBV (F = 47, P < 0.0001), corresponding to a regional difference in &Dgr;CBV when CO2 is changed. N2O inhalation did not significantly change the distribution of regional CBV (F = 2.4, P = 0.051) or &Dgr;CBV/&Dgr;CO2 in these nine subjects. Conclusions Nitrous oxide inhalation had no effect either on CBV or on the normal CBV–CO2 response in humans.