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Adenosine receptor dependent signaling is not obligatory for normobaric and hypobaric hypoxia-induced cerebral vasodilation in humans

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Author
Holland, Ryan
Bain, Anthony
Tymko, Michael
Rieger, Mathew
Howe, Connor
Willie, Christopher
Hansen, Alex
Fluck, Daniela
Wildfong, Kevin
Stembridge, Mike
Subedi, Prajan
Anholm, James
Ainslie, Philip
Date
2017-01-12
Acceptance date
2017-01-09
Type
Journal
Publisher
American Physiological Society
ISSN
8750-7587
Metadata
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Abstract
Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, placebo controlled design, was implemented to determine if adenosine receptor antagonism (theophylline, 3.75 mg/Kg) would reduce the CBF response to normobaric and hypobaric hypoxia. In 12 participants the partial pressures of end-tidal oxygen (PETO2) and carbon dioxide (PETCO2), ventilation (pneumotachography), blood pressure (finger-photoplethysmography), heart- rate (electrocardiogram), CBF (duplex ultrasound), and intra-cranial blood velocities (transcranial Doppler ultrasound) were measured during five-minute stages of isocapnic hypoxia at sea-level (98, 90, 80, & 70% SaO2). Ventilation, PETO2 and PETCO2, blood pressure, heart-rate and CBF were also measured upon exposure (128±31 minutes following arrival) to high-altitude (3800m) and six-hours following theophylline administration. At sea-level, although the CBF response to hypoxia was unaltered pre/post placebo, it was reduced following theophylline (P<0.01); a finding explained by a lower PETCO2 (P<0.01). Upon mathematical correction for PETCO2, the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e. response slope) was not different between trials, irrespective of PETCO2. At high-altitude, theophylline (n=6) had no effect on CBF compared to placebo (n=6) when end-tidal gases were comparable (P>0.05). We conclude that adenosine receptor dependent signaling is not obligatory for cerebral hypoxic vasodilation in humans.
Journal/conference proceeding
Journal of Applied Physiology
URI
http://hdl.handle.net/10369/8329
DOI
http://dx.doi.org/10.1152/japplphysiol.00840.2016
Rights
http://www.rioxx.net/licenses/all-rights-reserved
Sponsorship
Philip N. Ainslie was supported by a Canada Research Chair and NSERC Discovery grant. Ryan L. Hoiland was supported by an NSERC post-graduate award. Daniela Flück was supported by the Swiss National Science Foundation.
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