Nitrous oxide increases normocapnic cerebral blood flow velocity but does not affect the dynamic cerebrovascular response to step changes in end-tidal P(CO2) in humans.

Abstract

We sought to clarify the effect of nitrous oxide (N2O) on the immediate responses of cerebral vasculature to sudden changes in arterial carbon dioxide tension in healthy humans. By use of a transcranial Doppler ultrasonography, blood flow velocity in the middle cerebral artery (V(MCA)) was measured during a step increase followed by a step decrease in end-tidal CO2 tension (PET(CO2)) between normo- and hypercapnia while subjects inspired gas mixtures containing 70%O2 + 30% N2 (control) and 70% O2 + 30% N2O (N2O) separately. During the control condition, both step increase and decrease in PET(CO2) produced rapid exponential changes in V(MCA). An increase in V(MCA) produced by the step increase in PET(CO2) was smaller (P < 0.001) and slower (P < 0.001) than a decrease in V(MCA) induced by the step decrease in PET(CO2). These general features of the dynamic cerebrovascular response were not affected by substitution of N2O for N2 in the inspired gases although N2O increased baseline V(MCA) by 15% (P < 0.001) compared with the control condition. We conclude that N2(O) in itself does not affect the dynamic cerebrovascular response to arterial CO2 changes, although it produces static mild cerebral vasodilation. This study suggests that nitrous oxide does not affect the dynamic cerebrovascular reactivity to acute arterial carbon dioxide (CO2) changes, i.e., exponential changes in cerebral blood flow in response to step changes in alveolar CO2 tension, although it does produce a mild increase in normocapnic cerebral blood flow velocity.