Steady-state tilt has no effect on cerebrovascular CO2 reactivity in anterior and posterior cerebral circulations

Abstract

New Findings: What is the central question of this study? We investigated the effects of superimposed tilt and hypercapnia-induced cerebral arteriolar dilatation on anterior and posterior cerebrovascular CO2 reactivity using hyperoxic rebreathing in human participants. What is the main finding and its importance? The main findings are threefold: (i) cerebrovascular CO2 reactivity in the anterior and posterior cerebrovasculature is unchanged with tilt; (ii) cerebral autoregulation is unlikely responsible due to unchanging cerebrovascular resistance reactivity between positions; and (iii) cerebral blood flow is not pressure passive during tilt as it is with pharmacological or lower body negative pressure-induced changes in mean arterial pressure, suggesting that sympathetic activation or balanced transmural pressures during head-down tilt regulate cerebral blood flow. Cerebral autoregulation is a protective feature of the cerebrovasculature that maintains relatively constant cerebral perfusion in the face of static and dynamic fluctuations in mean arterial pressure (MAP). However, the extent that the cerebrovasculature can autoregulate in the face of superimposed steady-state orthostasis-induced changes in MAP (e.g. head-up and head-down tilt; HUT and HDT) and CO2-mediated arteriolar dilatation is unknown. We tested the effects of steady-state tilt on cerebrovascular CO2 reactivity in the middle and and posterior cerebral artery in the following five body positions: 90 deg HUT, 45 deg HUT, supine, 45 deg HDT and 90 deg HDT on a tilt table during a modified hyperoxic rebreathing test. Absolute and relative cerebrovascular CO2 reactivity [cerebral blood velocity (CBV)/CO2], cerebrovascular resistance (CVR) reactivity (CVR/CO2) and MAP reactivity (MAP/CO2) were quantified using linear regression. Mean arterial pressure was significantly elevated in 90 deg HDT compared with other positions during baseline steady-state tilt (P < 0.01). Absolute CBV/CO2 and CVR/CO2 were greater in the middle cerebral artery than the posterior cerebral artery (P < 0.01) in all body positions, but relative measures were not different (P = 0.143 and P = 0.360, respectively), nor was there any interaction with tilt position. In addition, there was no difference in absolute (P = 0.556) and relative MAP/CO2 (P = 0.308) between positions. Our data demonstrate that cerebral blood flow remains well regulated during superimposed steady-state orthostatic stress and dynamic changes in the partial pressure of end-tidal CO2 during rebreathing. Cerebral autoregulation is likely not the mechanism responsible, but rather sympathetic nervous system activation or a balanced cerebrovascular transmural pressure with HDT maintains resting cerebral blood flow and cerebrovascular CO2 reactivity during rebreathing.