Hyperoxic cerebral vasoconstriction in healthy humans: global, lobe, and regions of interest

Hyperoxia is used for hypoxia/ischemia-related conditions, but is associated with poorer clinical outcomes, potentially related to reductions in cerebral blood flow (CBF). Global CBF hyperoxia responses are variable; limited evidence suggests heightened sensitivity in anterior brain regions, leaving important gaps in understanding spatial resolution. Using 3-Tesla magnetic resonance imaging (MRI), we tested the hypotheses that 1) isocapnic hyperoxia would reduce CBF at the whole brain, gray matter (GM), and white matter (WM), and 2) this reduction would differ across all lobes. CBF was quantified using pseudo-continuous arterial spin labeling (pcASL) in 15 young adults (7 females) during normoxia followed by hyperoxia (∼80% O2). Data presented as means ± SD. End-tidal CO2 remained unchanged between conditions (P = 0.127), and blood pressure increased by 5 ± 6 mmHg (P = 0.013). Hyperoxia did not significantly reduce CBF at the whole brain, lobar, or any of the 65 brain regions of interest (ROIs; all P > 0.05). In contrast, whole brain cerebrovascular conductance (CVC) decreased by 12 ± 15%, (75 ± 20 to 66 ± 21 mL/100 g/min/100 mmHg; P = 0.011), with similar relative reductions in GM (13 ± 18%, 90 ± 24 to 78 ± 27 mL/100 g/min/100 mmHg; P = 0.021) and WM (8 ± 11%, 53 ± 14 to 49 ± 14 mL/100 g/min/100 mmHg; P = 0.013). CVC decreased across all lobes (9%-12%; all P < 0.05), with no inter-lobar differences (P = 0.866). Exploratory analyses showed reduced CVC in all 65 ROIs (3%-35%; all P < 0.026), but no regional heterogeneity was found within a given lobe (all P > 0.401). These new findings demonstrate widespread cerebral vasoconstriction without lobe- or region-specific effects during acute hyperoxia, providing a foundation for future studies involving greater hyperoxic exposure and clinically relevant populations.NEW & NOTEWORTHY This study demonstrates that acute isocapnic hyperoxia induces widespread cerebral vasoconstriction, reflected by reduced cerebrovascular conductance. Contrary to the hypothesis, the vasoconstrictive responses appear spatially uniform across lobes and regions of interest (ROIs), although the ROI conclusions are preliminary. These findings refine regional understanding of hyperoxia-induced cerebrovascular regulation and underscore the importance of considering vascular conductance, rather than CBF alone, when evaluating the cerebral effects of supplemental oxygen.