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Enhanced cerebral perfusion during brief exposures to cyclic intermittent hypoxemia.

Authors
  • Liu, Xiaoli1, 2
  • Xu, Diqun1
  • Hall, James R3
  • Ross, Sarah3
  • Chen, Shande3, 4
  • Liu, Howe5
  • Mallet, Robert T1
  • Shi, Xiangrong1, 4
  • 1 Institute of Cardiovascular & Metabolic Disease, University of North Texas Health Science Center , Fort Worth, Texas.
  • 2 Department of Physical Therapy, University of North Texas Health Science Center , Fort Worth, Texas.
  • 3 Hubei University for Nationalities, Enshi, Hubei , China. , (China)
  • 4 Institute of Healthy Aging, University of North Texas Health Science Center , Fort Worth, Texas.
  • 5 Department of Biostatistics, University of North Texas Health Science Center , Fort Worth, Texas.
Type
Published Article
Journal
Journal of Applied Physiology
Publisher
American Physiological Society
Publication Date
Dec 01, 2017
Volume
123
Issue
6
Pages
1689–1697
Identifiers
DOI: 10.1152/japplphysiol.00647.2017
PMID: 29074711
Source
Medline
Keywords
License
Unknown

Abstract

Cerebral vasodilation and increased cerebral oxygen extraction help maintain cerebral oxygen uptake in the face of hypoxemia. This study examined cerebrovascular responses to intermittent hypoxemia in eight healthy men breathing 10% O2 for 5 cycles, each 6 min, interspersed with 4 min of room air breathing. Hypoxia exposures raised heart rate ( P < 0.01) without altering arterial pressure, and increased ventilation ( P < 0.01) by expanding tidal volume. Arterial oxygen saturation ([Formula: see text]) and cerebral tissue oxygenation ([Formula: see text]) fell ( P < 0.01) less appreciably in the first bout (from 97.0 ± 0.3% and 72.8 ± 1.6% to 75.5 ± 0.9% and 54.5 ± 0.9%, respectively) than the fifth bout (from 94.9 ± 0.4% and 70.8 ± 1.0% to 66.7 ± 2.3% and 49.2 ± 1.5%, respectively). Flow velocity in the middle cerebral artery ( VMCA) and cerebrovascular conductance increased in a sigmoid fashion with decreases in [Formula: see text] and [Formula: see text]. These stimulus-response curves shifted leftward and upward from the first to the fifth hypoxia bouts; thus, the centering points fell from 79.2 ± 1.4 to 74.6 ± 1.1% ( P = 0.01) and from 59.8 ± 1.0 to 56.6 ± 0.3% ( P = 0.002), and the minimum VMCA increased from 54.0 ± 0.5 to 57.2 ± 0.5 cm/s ( P = 0.0001) and from 53.9 ± 0.5 to 57.1 ± 0.3 cm/s ( P = 0.0001) for the [Formula: see text]- VMCA and [Formula: see text]- VMCA curves, respectively. Cerebral oxygen extraction increased from prehypoxia 0.22 ± 0.01 to 0.25 ± 0.02 in minute 6 of the first hypoxia bout, and remained elevated between 0.25 ± 0.01 and 0.27 ± 0.01 throughout the fifth hypoxia bout. These results demonstrate that cerebral vasodilation combined with enhanced cerebral oxygen extraction fully compensated for decreased oxygen content during acute, cyclic hypoxemia. NEW & NOTEWORTHY Five bouts of 6-min intermittent hypoxia (IH) exposures to 10% O2 progressively reduce arterial oxygen saturation ([Formula: see text]) to 67% without causing discomfort or distress. Cerebrovascular responses to hypoxemia are dynamically reset over the course of a single IH session, such that threshold and saturation for cerebral vasodilations occurred at lower [Formula: see text] and cerebral tissue oxygenation ([Formula: see text]) during the fifth vs. first hypoxia bouts. Cerebral oxygen extraction is augmented during acute hypoxemia, which compensates for decreased arterial O2 content.

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