Cerebral vasoreactivity during hypercapnia is reset by augmented sympathetic influence

Abstract

Sympathetic nerve activity influences cerebral blood flow, but it is unknown whether augmented sympathetic nerve activity resets cerebral vasoreactivity to hypercapnia. This study tested the hypothesis that cerebral vasodilation during hypercapnia is restrained by lower-body negative pressure (LBNP)-stimulated sympathoexcitation. Cerebral hemodynamic responses were assessed in nine healthy volunteers [age 25 yr (SD 3)] during rebreathing-induced increases in partial pressure of end-tidal CO2 (PetCO2) at rest and during LBNP. Cerebral hemodynamic responses were determined by changes in flow velocity of middle cerebral artery (MCAV) using transcranial Doppler sonography and in regional cerebral tissue oxygenation (ScO2) using near-infrared spectroscopy. PetCO2 values during rebreathing were similarly increased from 41.9 to 56.5 mmHg at rest and from 40.7 to 56.0 mmHg during LBNP of −15 Torr. However, the rates of increases in MCAV and in ScO2 per unit increase in PetCO2 (i.e., the slopes of MCAV/PetCO2 and ScO2/PetCO2) were significantly ( P ≤0.05) decreased from 2.62 ± 0.16 cm·s−1·mmHg−1 and 0.89 ± 0.10%/mmHg at rest to 1.68 ± 0.18 cm·s−1·mmHg−1 and 0.63 ± 0.07%/mmHg during LBNP. In conclusion, the sensitivity of cerebral vasoreactivity to hypercapnia, in terms of the rate of increases in MCAV and in ScO2, is diminished by LBNP-stimulated sympathoexcitation.