Reactivity of Basilar and Circle of Willis Arteries Measured Simultaneously at 7 Tesla

The subcortical conduit vessels contribute significantly to the total cerebral vascular resistance making knowledge regarding their vasoreactivity to physiological stimuli a requirement when attempting to understand regional brain perfusion. Recent evidence points to significant dilatory and constrictor potential in the middle cerebral artery. However, reactivity of the remaining conduit arteries remains poorly understood due to a need for improved imaging methods that can assess these vessels simultaneously while each receives the same stimulus. In this study we characterize the basilar and all Circle of Willis conduit arteries' reactivity to changes in end‐tidal CO 2 (ETCO 2 ). All imaging was performed on a 7T Siemens MAGNETOM neuro‐optimized MRI using an 8‐channel transmit, 32‐channel receive head coil. Cross‐sectional area (%ΔCSA) measurements were evaluated from images collected using a T1‐weighted 3D SPACE pulse sequence, optimized to produce black‐blood and high signal contrast between vessel lumen and surrounding tissue. The acquisition was tuned to produce high‐resolution (0.5mm isotropic) information with no inflow signal (TE=8.2ms, TR=700ms, FOV=224mm sagittal, radial trajectory, iPat=2) and a whole‐brain acquisition time of 5.63 minutes. Collection of isotropic data allowed us to arbitrarily re‐orient the image data to evaluate the relative change in cross‐sectional area (%ΔCSA) of the subcortical conduit arteries perpendicular to the direction of flow. Change in ETCO 2 (ΔETCO 2, ADInstruments) and %ΔCSA data were produced from 7 healthy individuals (age range, 18–23 years). Cerebrovascular CO 2 reactivity was calculated as %ΔCSA/ΔETCO 2 . All 9 subcortical conduit arteries (basilar, right and left internal carotid, as well as the right and left posterior, middle and anterior cerebral arteries) were evaluated during normocapnia (37±6 mm Hg), hypercapnia (51±6 mmHg achieved by breathing a gas mixture of 5% CO 2 , balance oxygen), and hypocapnia (27±4 mmHg achieved by hyperventilation). Cerebral artery reactivity to hypercapnia exhibited a range of dilation from 0.27%/mm Hg in the right internal carotid artery to 2.5%/mm Hg in the left anterior cerebral artery. In response to hypocapnia, cerebral artery vasoconstriction ranged from 1.1%/mm Hg in the left anterior cerebral artery to 3.2%/mm Hg in the right posterior cerebral artery. This study demonstrated the heterogeneous cerebrovascular reactivity to hypercapnia and hypocapnia across the nine subcortical conduit arteries. Support or Funding Information Canadian Institute of Health Research (201503MOP‐342412‐MOV‐CEEA)