Regional hypoxic cerebral vasodilation facilitated by diameter changes primarily in anterior versus posterior circulation

Abstract

The inability to quantify cerebral blood flow and changes in macrocirculation cross-sectional area in all brain regions impedes robust insight into hypoxic cerebral blood flow control. We applied four-dimensional flow magnetic resonance imaging to quantify cerebral blood flow (ml • min-1) and cross-sectional area (mm2) simultaneously in 11 arteries. In healthy adults, blood pressure, O2 Saturation (SpO2), and end-tidal CO2 were measured at baseline and steady-state hypoxia (FiO2 = 0.11). We investigated left and right: internal carotid, vertebral, middle, anterior, posterior cerebral arteries, and basilar artery. Hypoxia (SpO2 = 80±2%) increased total cerebral blood flow from 621±38 to 742±50 ml • min-1 ( p < 0.05). Hypoxia increased cerebral blood flow, except in the right posterior cerebral arteries. Hypoxia increased cross-sectional area in the anterior arteries (left and right internal carotid arteries, left and right middle, p < 0.05; left and right anterior p = 0.08) but only the right vertebral artery of the posterior circulation. Nonetheless, relative cerebral blood flow distribution and vascular reactivity (Δ%cerebral blood flow • ΔSpO2-1) were not different between arteries. Collectively, moderate hypoxia: (1) increased cerebral blood flow, but relative distribution remains similar to normoxia, (2) evokes similar vascular reactivity between 11 arteries, and (3) increased cross-sectional area primarily in the anterior arteries. This study provides the first wide-ranging, quantitative, functional and structural data regarding intracranial arteries during hypoxia in humans, highlighting cerebral blood flow regulation of microcirculation and macrocirculation differs between anterior and posterior circulation.

Keywords: Cerebral blood flow; cerebral blood flow measurement; magnetic resonance imaging; physiology; vascular biology.

Figures

Figure 1.

Four-dimensional MRI- (PC VIPR) derived angiograms from a representative subject without contrast agent. Blue squares indicate cut-planes for 3.45 mm long measurements within a given vessel. (a) Coronal view, (b) Axial view, (c) Sagittal view of intracranial arteries segmented from the PC VIPR angiogram. Angiograms with overlaid velocity tracings along measurement points (d) Coronal view, (e) Axial view, and (f) Sagittal view. Arteries examined: ICA: right (r) and left (l) internal carotid artery; VA: right (r) and left (l) vertebral artery; BA: basilar artery; MCA: right (r) and left (l) middle cerebral artery; ACA: right (r) and left (l) anterior cerebral artery; PCA: right (r) and left (l) posterior cerebral artery.

Figure 2.

Cerebral blood flow quantified in 11 arteries supplying the brain. (a) absolute blood flow in each artery at baseline and hypoxia, (b) percent distribution of blood flow in each artery at baseline and hypoxia, and (c) percent change in blood flow from baseline. Data are mean ± SE, * indicates statistical significance from normoxia, p < 0.05. VA—r and VA—l n = 11.

Figure 3.

Hypoxic vascular reactivity in 11 arteries supplying the brain. (a) Absolute blood flow reactivity and (b) Relative blood flow reactivity. Data are means ± SE, #, significantly different than ICA—r,, significantly different than ICA—l, $, significantly different than MCA—r, p < 0.05. VA (r and l) n = 11.

Figure 4.

Hypoxia-induced change in cross-sectional area (CSA) from baseline. (a) Arteries of the anterior circulation and (b) Arteries of the posterior circulation. Data ± SE, * indicates Δ statistically significant p < 0.05. VA (r–l) n = 11.