Reactivity of larger intracranial arteries using 7 T MRI in young adults

Abstract

The larger intracranial conduit vessels contribute to the total cerebral vascular resistance, and understanding their vasoreactivity to physiological stimuli is required when attempting to understand regional brain perfusion. Reactivity of the larger cerebral conduit arteries remains understudied due to a need for improved imaging methods to simultaneously assess these vessels in a single stimulus. We characterized reactivity of basal intracranial conduit arteries (basilar, right and left posterior, middle and anterior cerebral arteries) and the right and left internal carotid arteries, to manipulations in end-tidal CO (PetCO). Cross-sectional area changes (%CSA) were evaluated from high-resolution (0.5 mm isotropic) images collected at 7 T using a T1-weighted 3D SPACE pulse sequence, providing high contrast between vessel lumen and surrounding tissue. Cerebrovascular reactivity was calculated as %CSA/ΔPetCO in eight healthy individuals (18-23 years) during normocapnia (41 ± 4 mmHg), hypercapnia (48 ± 4 mmHg; breathing 5% CO, balance oxygen), and hypocapnia (31 ± 8 mmHg; via hyperventilation). Reactivity to hypercapnia ranged from 0.8%/mmHg in the right internal carotid artery to 2.7%/mmHg in the left anterior cerebral artery. During hypocapnia, vasoconstriction ranged from 0.9%/mmHg in the basilar artery to 2.6%/mmHg in the right posterior cerebral artery. Heterogeneous cerebrovascular reactivity to hypercapnia and hypocapnia was characterized across basal intracranial conduit and internal carotid arteries.

Regulation of regional cerebral blood flow during graded reflex-mediated sympathetic activation via lower body negative pressure

“…The cerebral vasculature is highly sensitive to changes in arterial CO 2 (2,3). vasoconstriction and a reduction in CBF, whereas an increase in arterial CO 2 results in vasodilation and an increase in CBF (2,4,7,38). In the current study, there was a small but significant decrease in PET CO 2 during LBNP, indicating that some of the cerebral vasoconstriction could be due to the reduction in PET CO 2 .…”

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“…The reported vascular reactivity and autoregulation findings may differ depending on the context of the stimulus and analytical methods. Specifically, we reported vascular reactivity to hypercapnia; however, vasoreactivity to hypocapnia may produce different results than the current findings as reactivity differs between hypercapnia and hypocapnia in healthy humans (Coverdale et al ; Al‐Khazraji et al ). Our dynamic autoregulation findings in the MCA may not translate to other regions of the cerebrovasculature.…”

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“…In addition, this study was based on the usual assumption that the hypercapnic stimulus increased flow by dilation of downstream vessels without a meaningful increase in MCA diameter. Recent research supports dilation of the MCA (and other subcortical vessels) during hypercapnia of 46–48 mm Hg (Coverdale et al, ; Al‐Khazraji et al, 9). However, our participants did not exceed 45 mm Hg at any point.…”