Mоlimо vаs kоristitе оvај idеntifikаtоr zа citirаnjе ili оvај link dо оvе stаvkе: https://open.uns.ac.rs/handle/123456789/32475
Nаziv: Alterations in resting cerebrovascular regulation do not affect reactivity to hypoxia, hyperoxia or neurovascular coupling following a SCUBA dive
Аutоri: Hannah G Caldwell
Ryan L Hoiland
Otto Barak 
Tanja Mijacika
Joel S Burma
Željko Dujić
Philip N Ainslie
Ključnе rеči: Cerebrovascular Circulation;Duplex Ultrasound;SCUBA diving;Neurovascular Coupling;Hypoxia;Hyperoxia;Vasodilation
Dаtum izdаvаnjа: сеп-2020
Izdаvаč: Blackwell Publishing Ltd
Čаsоpis: Experimental Physiology
Sažetak: New Findings: What is the central question of this study? What are the characteristics of cerebral blood flow (CBF) regulation following a single SCUBA dive to a depth of 18 m sea water with a 47 min bottom time. What is the main finding and its importance? Acute alterations in CBF regulation at rest, including extra-cranial vasodilatation, reductions in shear patterns and elevations in intra-cranial blood velocity were observed at rest following a single SCUBA dive. These subtle changes in CBF regulation did not translate into any functional changes in cerebrovascular reactivity to hypoxia or hyperoxia, or neurovascular coupling following a single SCUBA dive. Abstract: Reductions in vascular function during a SCUBA dive – due to hyperoxia-induced oxidative stress, arterial and venous gas emboli and altered endothelial integrity – may also extend to the cerebrovasculature following return to the surface. This study aimed to characterize cerebral blood flow (CBF) regulation following a single SCUBA dive to a depth of 18 m sea water with a 47 min bottom time. Prior to and following the dive, participants (n = 11) completed (1) resting CBF in the internal carotid (ICA) and vertebral (VA) arteries (duplex ultrasound) and intra-cranial blood velocity (v) of the middle and posterior cerebral arteries (MCAv and PCAv, respectively) (transcranial Doppler ultrasound); (2) cerebrovascular reactivity to acute poikilocapnic hypoxia (i.e. (Formula presented.), 0.10) and hyperoxia (i.e. (Formula presented.), 1.0); and (3) neurovascular coupling (NVC; regional CBF response to local increases in cerebral metabolism). Global CBF, cerebrovascular reactivity to hypoxia and hyperoxia, and NVC were unaltered following a SCUBA dive (all P > 0.05); however, there were subtle changes in other cerebrovascular metrics post-dive, including reductions in ICA (−13 ± 8%, P = 0.003) and VA (−11 ± 14%, P = 0.021) shear rate, lower ICAv (−10 ± 9%, P = 0.008) and VAv (−9 ± 14%, P = 0.028), increases in ICA diameter (+4 ± 5%, P = 0.017) and elevations in PCAv (+10 ± 19%, P = 0.047). Although we observed subtle alterations in CBF regulation at rest, these changes did not translate into any functional changes in cerebrovascular reactivity to hypoxia or hyperoxia, or NVC. Whether prolonged exposure to hyperoxia and hyperbaria during longer, deeper, colder and/or repetitive SCUBA dives would provoke changes to the cerebrovasculature requires further investigation.
URI: https://open.uns.ac.rs/handle/123456789/32475
ISSN: 09580670
DOI: 10.1113/EP088746
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