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Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure
The ability to maintain adequate cerebral blood flow and oxygenation determines tolerance to central hypovolemia. We tested the hypothesis that acute hypoxemia during simulated blood loss in humans would cause impairments in cerebral blood flow control. Ten healthy subjects (32 ± 6 years, BMI 27 ± 2...
Main Authors: | , , , , , , , , , |
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Format: | Online Article Text |
Language: | English |
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John Wiley and Sons Inc.
2018
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Subjects: | |
Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820424/ https://www.ncbi.nlm.nih.gov/pubmed/29464923 http://dx.doi.org/10.14814/phy2.13594 |
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author | van Helmond, Noud Johnson, Blair D. Holbein, Walter W. Petersen‐Jones, Humphrey G. Harvey, Ronée E. Ranadive, Sushant M. Barnes, Jill N. Curry, Timothy B. Convertino, Victor A. Joyner, Michael J. |
author_facet | van Helmond, Noud Johnson, Blair D. Holbein, Walter W. Petersen‐Jones, Humphrey G. Harvey, Ronée E. Ranadive, Sushant M. Barnes, Jill N. Curry, Timothy B. Convertino, Victor A. Joyner, Michael J. |
author_sort | van Helmond, Noud |
collection | PubMed |
description | The ability to maintain adequate cerebral blood flow and oxygenation determines tolerance to central hypovolemia. We tested the hypothesis that acute hypoxemia during simulated blood loss in humans would cause impairments in cerebral blood flow control. Ten healthy subjects (32 ± 6 years, BMI 27 ± 2 kg·m(−2)) were exposed to stepwise lower body negative pressure (LBNP, 5 min at 0, −15, −30, and −45 mmHg) during both normoxia and hypoxia (F(i)O(2) = 0.12–0.15 O(2) titrated to an SaO(2) of ~85%). Physiological responses during both protocols were expressed as absolute changes from baseline, one subject was excluded from analysis due to presyncope during the first stage of LBNP during hypoxia. LBNP induced greater reductions in mean arterial pressure during hypoxia versus normoxia (MAP, at −45 mmHg: −20 ± 3 vs. −5 ± 3 mmHg, P < 0.01). Despite differences in MAP, middle cerebral artery velocity responses (MCAv) were similar between protocols (P = 0.41) due to increased cerebrovascular conductance index (CVCi) during hypoxia (main effect, P = 0.04). Low frequency MAP (at −45 mmHg: 17 ± 5 vs. 0 ± 5 mmHg(2), P = 0.01) and MCAv (at −45 mmHg: 4 ± 2 vs. −1 ± 1 cm·s(−2), P = 0.04) spectral power density, as well as low frequency MAP‐mean MCAv transfer function gain (at −30 mmHg: 0.09 ± 0.06 vs. −0.07 ± 0.06 cm·s(−1)·mmHg(−1), P = 0.04) increased more during hypoxia versus normoxia. Contrary to our hypothesis, these findings support the notion that cerebral blood flow control is not impaired during exposure to acute hypoxia and progressive central hypovolemia despite lower MAP as a result of compensated increases in cerebral conductance and flow variability. |
format | Online Article Text |
id | pubmed-5820424 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-58204242018-02-26 Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure van Helmond, Noud Johnson, Blair D. Holbein, Walter W. Petersen‐Jones, Humphrey G. Harvey, Ronée E. Ranadive, Sushant M. Barnes, Jill N. Curry, Timothy B. Convertino, Victor A. Joyner, Michael J. Physiol Rep Original Research The ability to maintain adequate cerebral blood flow and oxygenation determines tolerance to central hypovolemia. We tested the hypothesis that acute hypoxemia during simulated blood loss in humans would cause impairments in cerebral blood flow control. Ten healthy subjects (32 ± 6 years, BMI 27 ± 2 kg·m(−2)) were exposed to stepwise lower body negative pressure (LBNP, 5 min at 0, −15, −30, and −45 mmHg) during both normoxia and hypoxia (F(i)O(2) = 0.12–0.15 O(2) titrated to an SaO(2) of ~85%). Physiological responses during both protocols were expressed as absolute changes from baseline, one subject was excluded from analysis due to presyncope during the first stage of LBNP during hypoxia. LBNP induced greater reductions in mean arterial pressure during hypoxia versus normoxia (MAP, at −45 mmHg: −20 ± 3 vs. −5 ± 3 mmHg, P < 0.01). Despite differences in MAP, middle cerebral artery velocity responses (MCAv) were similar between protocols (P = 0.41) due to increased cerebrovascular conductance index (CVCi) during hypoxia (main effect, P = 0.04). Low frequency MAP (at −45 mmHg: 17 ± 5 vs. 0 ± 5 mmHg(2), P = 0.01) and MCAv (at −45 mmHg: 4 ± 2 vs. −1 ± 1 cm·s(−2), P = 0.04) spectral power density, as well as low frequency MAP‐mean MCAv transfer function gain (at −30 mmHg: 0.09 ± 0.06 vs. −0.07 ± 0.06 cm·s(−1)·mmHg(−1), P = 0.04) increased more during hypoxia versus normoxia. Contrary to our hypothesis, these findings support the notion that cerebral blood flow control is not impaired during exposure to acute hypoxia and progressive central hypovolemia despite lower MAP as a result of compensated increases in cerebral conductance and flow variability. John Wiley and Sons Inc. 2018-02-21 /pmc/articles/PMC5820424/ /pubmed/29464923 http://dx.doi.org/10.14814/phy2.13594 Text en © 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research van Helmond, Noud Johnson, Blair D. Holbein, Walter W. Petersen‐Jones, Humphrey G. Harvey, Ronée E. Ranadive, Sushant M. Barnes, Jill N. Curry, Timothy B. Convertino, Victor A. Joyner, Michael J. Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
title | Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
title_full | Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
title_fullStr | Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
title_full_unstemmed | Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
title_short | Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
title_sort | effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820424/ https://www.ncbi.nlm.nih.gov/pubmed/29464923 http://dx.doi.org/10.14814/phy2.13594 |
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