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

Autor:	Hoiland RL; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada; ryanleohoiland@gmail.com., Bain AR; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Tymko MM; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Rieger MG; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Howe CA; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Willie CK; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Hansen AB; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Flück D; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Wildfong KW; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada., Stembridge M; Cardiff Centre for Exercise and Health, Cardiff Metropolitan University, Cardiff, United Kingdom; and., Subedi P; VA Loma Linda Healthcare System and Loma Linda University School of Medicine, Loma Linda, California., Anholm J; VA Loma Linda Healthcare System and Loma Linda University School of Medicine, Loma Linda, California., Ainslie PN; Centre for Heart, Lung and Vascular Health, University of British Columbia, Okanagan Campus, School of Health and Exercise Sciences, Kelowna, British Columbia, Canada.
Jazyk:	angličtina
Zdroj:	Journal of applied physiology (Bethesda, Md. : 1985) [J Appl Physiol (1985)] 2017 Apr 01; Vol. 122 (4), pp. 795-808. Date of Electronic Publication: 2017 Jan 12.
DOI:	10.1152/japplphysiol.00840.2016
Abstrakt:	Hypoxia increases cerebral blood flow (CBF) with the underlying signaling processes potentially including adenosine. A randomized, double-blinded, and 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 ([Formula: see text]) and carbon dioxide ([Formula: see text]), ventilation (pneumotachography), blood pressure (finger photoplethysmography), heart rate (electrocardiogram), CBF (duplex ultrasound), and intracranial blood velocities (transcranial Doppler ultrasound) were measured during 5-min stages of isocapnic hypoxia at sea level (98, 90, 80, and 70% [Formula: see text]). Ventilation, [Formula: see text] and [Formula: see text], blood pressure, heart rate, and CBF were also measured upon exposure (128 ± 31 min following arrival) to high altitude (3,800 m) and 6 h following theophylline administration. At sea level, although the CBF response to hypoxia was unaltered pre- and postplacebo, it was reduced following theophylline ( P < 0.01), a finding explained by a lower [Formula: see text] ( P < 0.01). Upon mathematical correction for [Formula: see text], the CBF response to hypoxia was unaltered following theophylline. Cerebrovascular reactivity to hypoxia (i.e., response slope) was not different between trials, irrespective of [Formula: see text] At high altitude, theophylline ( n = 6) had no effect on CBF compared with 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. NEW & NOTEWORTHY The signaling pathways that regulate human cerebral blood flow in hypoxia remain poorly understood. Using a randomized, double-blinded, and placebo-controlled study design, we determined that adenosine receptor-dependent signaling is not obligatory for the regulation of human cerebral blood flow at sea level; these findings also extend to high altitude. (Copyright © 2017 the American Physiological Society.)
Databáze:	MEDLINE
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