- Library Home /
- Search Collections /
- Open Collections /
- Browse Collections /
- UBC Faculty Research and Publications /
- Acute intermittent hypercapnic hypoxia and sympathetic...
Open Collections
UBC Faculty Research and Publications
Acute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in men Stuckless, Troy J. R.; Vermeulen, Tyler D.; Brown, Courtney V.; Boulet, Lindsey M.; Shafer, Brooke M.; Wakeham, Denis J.; Steinback, Craig D.; Ayas, Najib T.; Floras, John S.; Foster, Glen E.
Abstract
Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations in sympathetic vasomotor outflow and blood pressure in healthy humans. It is unknown whether IH alters sympathetic neurovascular transduction (sNVT), measured as the relationship between sympathetic vasomotor outflow and either forearm vascular conductance (FVC; regional sNVT) or diastolic blood pressure (DBP; systemic sNVT). We tested the hypothesis that IH augments sNVT by exposing healthy males to 40 consecutive 1-minute breathing cycles, each comprising 40-seconds of hypercapnic hypoxia (PETCO₂: +4±3 mm Hg above baseline; PETO₂: 48±3 mm Hg) and 20-seconds of normoxia (n=9), or a 40-minute air-breathing control (n=7). Before and after the intervention, lower body negative pressure (LBNP; 3 minutes at -15, -30, and -45 mmHg) was applied to elicit reflex increases in muscle sympathetic nerve activity (MSNA, fibular microneurography) while clamping end-tidal gases at baseline levels. Ventilation, arterial pressure (SBP, DBP, MAP), brachial artery blood flow (Q̇ BA), FVC (Q̇ BA/MAP), and MSNA burst frequency were measured continuously. Following IH, but not control, ventilation (5 l/min; 95% CI: 1 - 9), and MAP (5 mmHg; 95% CI: 1 - 9) were increased, while FVC (-0.2 ml/min/mm Hg; 95% CI: -0.0 - -0.4) and mean shear rate (SR; -21.9 /s; 95% CI: -5.8 - -38.0; all P<0.05) were reduced. Systemic sNVT was increased following IH (0.25 mm Hg/burst/min; 95% CI: 0.01 – 0.49; P<0.05), while changes in regional forearm sNVT were similar between IH and sham. Reductions in vessel wall shear stress and consequently nitric oxide production, may contribute to heightened systemic sNVT and provide a potential neuro-vascular mechanism for elevated blood pressure in obstructive sleep apnoea.
Item Metadata
Title |
Acute intermittent hypercapnic hypoxia and sympathetic neurovascular transduction in men
|
Alternate Title |
Intermittent Hypoxia and Sympathetic Neurovascular Transduction
|
Creator | |
Contributor | |
Description |
Acute intermittent hypercapnic hypoxia (IH) induces long-lasting elevations in sympathetic
vasomotor outflow and blood pressure in healthy humans. It is unknown whether IH alters
sympathetic neurovascular transduction (sNVT), measured as the relationship between
sympathetic vasomotor outflow and either forearm vascular conductance (FVC; regional sNVT)
or diastolic blood pressure (DBP; systemic sNVT). We tested the hypothesis that IH augments
sNVT by exposing healthy males to 40 consecutive 1-minute breathing cycles, each comprising
40-seconds of hypercapnic hypoxia (PETCO₂: +4±3 mm Hg above baseline; PETO₂: 48±3 mm
Hg) and 20-seconds of normoxia (n=9), or a 40-minute air-breathing control (n=7). Before and
after the intervention, lower body negative pressure (LBNP; 3 minutes at -15, -30, and -45
mmHg) was applied to elicit reflex increases in muscle sympathetic nerve activity (MSNA,
fibular microneurography) while clamping end-tidal gases at baseline levels. Ventilation, arterial
pressure (SBP, DBP, MAP), brachial artery blood flow (Q̇ BA), FVC (Q̇ BA/MAP), and MSNA
burst frequency were measured continuously. Following IH, but not control, ventilation (5 l/min;
95% CI: 1 - 9), and MAP (5 mmHg; 95% CI: 1 - 9) were increased, while FVC (-0.2 ml/min/mm
Hg; 95% CI: -0.0 - -0.4) and mean shear rate (SR; -21.9 /s; 95% CI: -5.8 - -38.0; all P<0.05)
were reduced. Systemic sNVT was increased following IH (0.25 mm Hg/burst/min; 95% CI:
0.01 – 0.49; P<0.05), while changes in regional forearm sNVT were similar between IH and
sham. Reductions in vessel wall shear stress and consequently nitric oxide production, may
contribute to heightened systemic sNVT and provide a potential neuro-vascular mechanism for
elevated blood pressure in obstructive sleep apnoea.
|
Subject | |
Genre | |
Type | |
Language |
eng
|
Date Available |
2021-12-31
|
Provider |
Vancouver : University of British Columbia Library
|
Rights |
Attribution-NonCommercial-NoDerivatives 4.0 International
|
DOI |
10.14288/1.0389549
|
URI | |
Affiliation | |
Peer Review Status |
Reviewed
|
Scholarly Level |
Faculty
|
Rights URI | |
Aggregated Source Repository |
DSpace
|
Item Media
Item Citations and Data
Rights
Attribution-NonCommercial-NoDerivatives 4.0 International