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

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