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Publication Alert! IALH Research Fellow Kurt Smith has co-authored a new research article entitled Exercise and Hypercapnia Differentially Modify Ratios of Extracranial and Intracranial Pulsatility. Other authors include Noah DuBose, Philip N. Ainslie, Sara R. Sherman, Tracy Baynard, Ryan Hoiland, and Daniel J. Green. The article was published in FASEB journal : official publication of the Federation of American Societies for Experimental Biology.
Abstract:
INTRODUCTION: Damping of pulsatile flow between extracranial and intracranial cerebral arteries is an essential allostatic mechanism protecting cerebral microvessels from recalcitrant hemodynamics. The ratio of pulsatility between proximal and distal cerebral arteries may provide a measure of cerebrovascular hemodynamic damping. This might prove useful as an evaluation of cerebrovascular regulation in response to pulsatile perturbations.
PURPOSE: To characterize cerebral pulsatile damping between extracranial and intracranial environments in response to perturbations eliciting matched shear stress, such as exercise and hypercapnia.
METHODS: Participants (n=10) completed two 30-min experimental conditions aimed at matching cerebral artery shear stress, each separated by 48 hrs: (1) mild hypercapnia (CO2 ; FI CO2 :0.045) and (2) submaximal cycling (EX; 60%HRreserve). Cerebral pulsatility index (PI: (systolic velocity-diastolic velocity)/mean velocity)) was assessed at baseline, during, and following each condition in the internal carotid artery (ICA) and middle cerebral artery (MCA) using Doppler ultrasound. Heart rate (HR) and blood pressure (BP) were assessed continuously using ECG and photoplethysmography, respectively. Cerebral pulsatile damping was calculated: (ICA PI / MCA PI) to investigate ratios of cerebral pulsatile hemodynamics between extracranial and intracranial arteries.
RESULTS: Cerebral pulsatile damping was greater during CO2 (1.66 ± 0.31) than EX (1.22 ± 0.35) (time*condition effect, p=0.002). The change in cerebral pulsatile damping was related to the change in heart rate (r = -0.70, p = 0.04), but not BP between baseline and the experimental conditions.
CONCLUSIONS: As evidenced by the response in cerebral pulsatile damping, exercise and hypercapnia result in different ratios of extracranial to intracranial pulsatility despite inducing similar vasodilation when shear stress was matched. This might in part be explained by differences in HR between conditions. Further research is important to elucidate the mechanisms behind the deviance in hemodynamic responses. © FASEB.
To read the full article, see https://faseb.onlinelibrary.wiley.com/doi/10.1096/fasebj.2022.36.S1.R5027
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