Nitrous oxide increases normocapnic cerebral blood flow velocity but does not affect the dynamic cerebrovascular response to step changes in end-tidal Pco(2) in humans

We sought to clarify the effect of nitrous oxide (N2O) on the immediate res ponses of cerebral vasculature to sudden changes in arterial carbon dioxide tension in healthy humans. By use of a transcranial Doppler ultrasonograph y, blood flow velocity in the middle cerebral artery (V-MCA) was measured d uring a step increase followed by a step decrease in end-tidal CO2 tension (PETCO2) between normo- and hypercapnia while subjects inspired gas mixture s containing 70% O-2 + 30% N-2 (control) and 70% O-2 + 30% N2O (N2O) separa tely. During the control condition, both step increase and decrease in PETC O2 Produced rapid exponential changes in V-MCA. An increase in V-MCA produc ed by the step increase in PETCO2 was Smaller (P < 0.001) and slower (P < 0 .001) than a decrease in V-MCA induced by the step decrease in PETCO2. Thes e general features of the dynamic cerebrovascular response were not affecte d by substitution of N2O for N-2 in the inspired gases although N2O increas ed baseline V-MCA by 15% (P < 0.001) compared with the control condition. W e conclude that N2O in itself does not affect the dynamic cerebrovascular r esponse to arterial CO2 changes, although it produces static mild cerebral vasodilation. Implications: This study suggests that nitrous oxide does not affect the dynamic cerebrovascular reactivity to acute arterial carbon dio xide (CO2) changes, i.e., exponential changes in cerebral blood flow in res ponse to step changes in alveolar CO2 tension, although it does produce a m ild increase in normocapnic cerebral blood flow velocity.