Matched increases in cerebral artery shear stress, irrespective of stimulus, induce similar changes in extra-cranial arterial diameter in humans: J Cereb Blood Flow Metab

K. J. Smith, Ryan L. Hoiland, R. Grove, H. McKirdy, L. Naylor, Philip N. Ainslie, D. J. Green

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Abstract

The mechanistic role of arterial shear stress in the regulation of cerebrovascular responses to physiological stimuli (exercise and hypercapnia) is poorly understood. We hypothesised that, if shear stress is a key regulator of arterial dilation, then matched increases in shear, induced by distinct physiological stimuli, would trigger similar dilation of the large extra-cranial arteries. Participants ( n = 10) participated in three 30-min experimental interventions, each separated by >/=48 h: (1) mild-hypercapnia (FICO2: approximately 0.045); (2) submaximal cycling (EX; 60%HRreserve); or (3) resting (time-matched control, CTRL). Blood flow, diameter, and shear rate were assessed (via Duplex ultrasound) in the internal carotid and vertebral arteries (ICA, VA) at baseline, during and following the interventions. Hypercapnia and EX produced similar elevations in blood flow and shear rate through the ICA and VA ( p <0.001), which were both greater than CTRL. Vasodilation of ICA and VA diameter in response to hypercapnia (5.3 +/- 0.8 and 4.4 +/- 2.0%) and EX (4.7 +/- 0.7 and 4.7 +/- 2.2%) were similar, and greater than CTRL ( p <0.001). Our findings indicate that matched levels of shear, irrespective of their driving stimulus, induce similar extra-cranial artery dilation. We demonstrate, for the first time in humans, an important mechanistic role for the endothelium in regulating cerebrovascular response to common physiological stimuli in vivo.
Original languageEnglish
Number of pages10
JournalJournal of Cerebral Blood Flow and Metabolism
Volume39
Issue number5
Early online date10 Nov 2017
DOIs
Publication statusPublished - May 2019

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Cerebral Arteries
Hypercapnia
Dilatation
Arteries
Vertebral Artery
Internal Carotid Artery
Vasodilation
Endothelium

Cite this

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title = "Matched increases in cerebral artery shear stress, irrespective of stimulus, induce similar changes in extra-cranial arterial diameter in humans: J Cereb Blood Flow Metab",
abstract = "The mechanistic role of arterial shear stress in the regulation of cerebrovascular responses to physiological stimuli (exercise and hypercapnia) is poorly understood. We hypothesised that, if shear stress is a key regulator of arterial dilation, then matched increases in shear, induced by distinct physiological stimuli, would trigger similar dilation of the large extra-cranial arteries. Participants ( n = 10) participated in three 30-min experimental interventions, each separated by >/=48 h: (1) mild-hypercapnia (FICO2: approximately 0.045); (2) submaximal cycling (EX; 60{\%}HRreserve); or (3) resting (time-matched control, CTRL). Blood flow, diameter, and shear rate were assessed (via Duplex ultrasound) in the internal carotid and vertebral arteries (ICA, VA) at baseline, during and following the interventions. Hypercapnia and EX produced similar elevations in blood flow and shear rate through the ICA and VA ( p <0.001), which were both greater than CTRL. Vasodilation of ICA and VA diameter in response to hypercapnia (5.3 +/- 0.8 and 4.4 +/- 2.0{\%}) and EX (4.7 +/- 0.7 and 4.7 +/- 2.2{\%}) were similar, and greater than CTRL ( p <0.001). Our findings indicate that matched levels of shear, irrespective of their driving stimulus, induce similar extra-cranial artery dilation. We demonstrate, for the first time in humans, an important mechanistic role for the endothelium in regulating cerebrovascular response to common physiological stimuli in vivo.",
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T1 - Matched increases in cerebral artery shear stress, irrespective of stimulus, induce similar changes in extra-cranial arterial diameter in humans

T2 - J Cereb Blood Flow Metab

AU - Smith, K. J.

AU - Hoiland, Ryan L.

AU - Grove, R.

AU - McKirdy, H.

AU - Naylor, L.

AU - Ainslie, Philip N.

AU - Green, D. J.

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N2 - The mechanistic role of arterial shear stress in the regulation of cerebrovascular responses to physiological stimuli (exercise and hypercapnia) is poorly understood. We hypothesised that, if shear stress is a key regulator of arterial dilation, then matched increases in shear, induced by distinct physiological stimuli, would trigger similar dilation of the large extra-cranial arteries. Participants ( n = 10) participated in three 30-min experimental interventions, each separated by >/=48 h: (1) mild-hypercapnia (FICO2: approximately 0.045); (2) submaximal cycling (EX; 60%HRreserve); or (3) resting (time-matched control, CTRL). Blood flow, diameter, and shear rate were assessed (via Duplex ultrasound) in the internal carotid and vertebral arteries (ICA, VA) at baseline, during and following the interventions. Hypercapnia and EX produced similar elevations in blood flow and shear rate through the ICA and VA ( p <0.001), which were both greater than CTRL. Vasodilation of ICA and VA diameter in response to hypercapnia (5.3 +/- 0.8 and 4.4 +/- 2.0%) and EX (4.7 +/- 0.7 and 4.7 +/- 2.2%) were similar, and greater than CTRL ( p <0.001). Our findings indicate that matched levels of shear, irrespective of their driving stimulus, induce similar extra-cranial artery dilation. We demonstrate, for the first time in humans, an important mechanistic role for the endothelium in regulating cerebrovascular response to common physiological stimuli in vivo.

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