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Interactions between CO2 chemoreflexes and arterial baroreflexes
Departments of Medicine and Physiology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center, and Medical College of Virginia of Virginia Commonwealth University, Richmond, Virginia 23249 We studied interactions between CO 2 chemoreflexes and arterial baroreflexes in 10 supine healthy...
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Published in: | American journal of physiology. Heart and circulatory physiology 1998-06, Vol.274 (6), p.H2177 |
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container_issue | 6 |
container_start_page | H2177 |
container_title | American journal of physiology. Heart and circulatory physiology |
container_volume | 274 |
creator | Henry, Rebecca A Lu, I-Li Beightol, Larry A Eckberg, Dwain L |
description | Departments of Medicine and Physiology, Hunter Holmes McGuire
Department of Veterans Affairs Medical Center, and Medical College of
Virginia of Virginia Commonwealth University, Richmond, Virginia
23249
We studied interactions between
CO 2 chemoreflexes and arterial
baroreflexes in 10 supine healthy young men and women. We measured vagal carotid baroreceptor-cardiac reflexes and steady-state fast Fourier transform R-R interval and photoplethysmographic arterial pressure power spectra at three arterial pressure levels
(nitroprusside, saline, and phenylephrine infusions) and three
end-tidal CO 2 levels (3, 4, and
5%, fixed-frequency, large-tidal-volume breathing, CO 2 plus
O 2 ). Our study supports three
principal conclusions. First, although low levels of
CO 2 chemoreceptor stimulation
reduce R-R intervals and R-R interval variability, statistical modeling suggests that this effect is indirect rather than direct
and is mediated by reductions of arterial pressure. Second, reductions of R-R intervals during hypocapnia reflect simple shifting of vagally
mediated carotid baroreflex responses on the R-R interval axis rather
than changes of baroreflex gain, range, or operational point. Third,
the influence of CO 2 chemoreceptor
stimulation on arterial pressure (and, derivatively, on R-R intervals
and R-R interval variability) depends critically on baseline arterial pressure levels: chemoreceptor effects are smaller when pressure is low
and larger when arterial pressure is high.
defense reaction; vagal baroreceptor; sympathetic innervation; hyperventilation |
doi_str_mv | 10.1152/ajpheart.1998.274.6.h2177 |
format | article |
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Department of Veterans Affairs Medical Center, and Medical College of
Virginia of Virginia Commonwealth University, Richmond, Virginia
23249
We studied interactions between
CO 2 chemoreflexes and arterial
baroreflexes in 10 supine healthy young men and women. We measured vagal carotid baroreceptor-cardiac reflexes and steady-state fast Fourier transform R-R interval and photoplethysmographic arterial pressure power spectra at three arterial pressure levels
(nitroprusside, saline, and phenylephrine infusions) and three
end-tidal CO 2 levels (3, 4, and
5%, fixed-frequency, large-tidal-volume breathing, CO 2 plus
O 2 ). Our study supports three
principal conclusions. First, although low levels of
CO 2 chemoreceptor stimulation
reduce R-R intervals and R-R interval variability, statistical modeling suggests that this effect is indirect rather than direct
and is mediated by reductions of arterial pressure. Second, reductions of R-R intervals during hypocapnia reflect simple shifting of vagally
mediated carotid baroreflex responses on the R-R interval axis rather
than changes of baroreflex gain, range, or operational point. Third,
the influence of CO 2 chemoreceptor
stimulation on arterial pressure (and, derivatively, on R-R intervals
and R-R interval variability) depends critically on baseline arterial pressure levels: chemoreceptor effects are smaller when pressure is low
and larger when arterial pressure is high.
defense reaction; vagal baroreceptor; sympathetic innervation; hyperventilation</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.1998.274.6.h2177</identifier><identifier>PMID: 9841543</identifier><language>eng</language><ispartof>American journal of physiology. Heart and circulatory physiology, 1998-06, Vol.274 (6), p.H2177</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Henry, Rebecca A</creatorcontrib><creatorcontrib>Lu, I-Li</creatorcontrib><creatorcontrib>Beightol, Larry A</creatorcontrib><creatorcontrib>Eckberg, Dwain L</creatorcontrib><title>Interactions between CO2 chemoreflexes and arterial baroreflexes</title><title>American journal of physiology. Heart and circulatory physiology</title><description>Departments of Medicine and Physiology, Hunter Holmes McGuire
Department of Veterans Affairs Medical Center, and Medical College of
Virginia of Virginia Commonwealth University, Richmond, Virginia
23249
We studied interactions between
CO 2 chemoreflexes and arterial
baroreflexes in 10 supine healthy young men and women. We measured vagal carotid baroreceptor-cardiac reflexes and steady-state fast Fourier transform R-R interval and photoplethysmographic arterial pressure power spectra at three arterial pressure levels
(nitroprusside, saline, and phenylephrine infusions) and three
end-tidal CO 2 levels (3, 4, and
5%, fixed-frequency, large-tidal-volume breathing, CO 2 plus
O 2 ). Our study supports three
principal conclusions. First, although low levels of
CO 2 chemoreceptor stimulation
reduce R-R intervals and R-R interval variability, statistical modeling suggests that this effect is indirect rather than direct
and is mediated by reductions of arterial pressure. Second, reductions of R-R intervals during hypocapnia reflect simple shifting of vagally
mediated carotid baroreflex responses on the R-R interval axis rather
than changes of baroreflex gain, range, or operational point. Third,
the influence of CO 2 chemoreceptor
stimulation on arterial pressure (and, derivatively, on R-R intervals
and R-R interval variability) depends critically on baseline arterial pressure levels: chemoreceptor effects are smaller when pressure is low
and larger when arterial pressure is high.
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Department of Veterans Affairs Medical Center, and Medical College of
Virginia of Virginia Commonwealth University, Richmond, Virginia
23249
We studied interactions between
CO 2 chemoreflexes and arterial
baroreflexes in 10 supine healthy young men and women. We measured vagal carotid baroreceptor-cardiac reflexes and steady-state fast Fourier transform R-R interval and photoplethysmographic arterial pressure power spectra at three arterial pressure levels
(nitroprusside, saline, and phenylephrine infusions) and three
end-tidal CO 2 levels (3, 4, and
5%, fixed-frequency, large-tidal-volume breathing, CO 2 plus
O 2 ). Our study supports three
principal conclusions. First, although low levels of
CO 2 chemoreceptor stimulation
reduce R-R intervals and R-R interval variability, statistical modeling suggests that this effect is indirect rather than direct
and is mediated by reductions of arterial pressure. Second, reductions of R-R intervals during hypocapnia reflect simple shifting of vagally
mediated carotid baroreflex responses on the R-R interval axis rather
than changes of baroreflex gain, range, or operational point. Third,
the influence of CO 2 chemoreceptor
stimulation on arterial pressure (and, derivatively, on R-R intervals
and R-R interval variability) depends critically on baseline arterial pressure levels: chemoreceptor effects are smaller when pressure is low
and larger when arterial pressure is high.
defense reaction; vagal baroreceptor; sympathetic innervation; hyperventilation</abstract><pmid>9841543</pmid><doi>10.1152/ajpheart.1998.274.6.h2177</doi></addata></record> |
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source | American Physiological Society Free |
title | Interactions between CO2 chemoreflexes and arterial baroreflexes |
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