Abstract
We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO2), and to normoxic hypercapnia. Oxygen saturation (SaO2), end-tidal CO2 (et-CO2), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O2: -0.33 ± 0.05, -0.74 ± 0.02 and -1.59 ± 0.3, p <0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO2, whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO2. We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.
| Original language | English |
|---|---|
| Pages (from-to) | 373-381 |
| Number of pages | 9 |
| Journal | Clinical Autonomic Research |
| Volume | 15 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Dec 2005 |
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Keywords
- Baroreflex
- Cerebral circulation
- Chemoreflex
- Hypercapnia
- Hypoxia
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
Interaction between central-peripheral chemoreflexes and cerebro-cardiovascular control. / Spicuzza, Lucia; Porta, Cesare; Bramanti, Alfina; Maffeis, Mara; Casucci, Gaia; Casiraghi, Nadia; Bernardi, Luciano.
In: Clinical Autonomic Research, Vol. 15, No. 6, 12.2005, p. 373-381.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Interaction between central-peripheral chemoreflexes and cerebro-cardiovascular control
AU - Spicuzza, Lucia
AU - Porta, Cesare
AU - Bramanti, Alfina
AU - Maffeis, Mara
AU - Casucci, Gaia
AU - Casiraghi, Nadia
AU - Bernardi, Luciano
PY - 2005/12
Y1 - 2005/12
N2 - We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO2), and to normoxic hypercapnia. Oxygen saturation (SaO2), end-tidal CO2 (et-CO2), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O2: -0.33 ± 0.05, -0.74 ± 0.02 and -1.59 ± 0.3, p <0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO2, whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO2. We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.
AB - We investigated the interaction between hypoxia and hypercapnia on ventilation and on cerebro-cardio-vascular control. A group of 12 healthy subjects performed rebreathing tests to determine the ventilatory response to hypoxia, at different levels of carbon dioxide (CO2), and to normoxic hypercapnia. Oxygen saturation (SaO2), end-tidal CO2 (et-CO2), minute ventilation, blood pressure, R-R interval and mid-cerebral artery flow velocity (MCFV) were continuously recorded. The hypoxic ventilatory response significantly increased under hypercapnia and decreased under hypocapnia (slopes L/min/% Sa O2: -0.33 ± 0.05, -0.74 ± 0.02 and -1.59 ± 0.3, p <0.0001, in hypocapnia, normocapnia and hypercapnia, respectively). At similar degrees of ventilation, MCFV increased more markedly during normocapnic hypoxia than normoxic hypercapnia; the slopes linking MCFV to hypoxia remained unchanged at increasing levels of et-CO2, whereas the regression lines were shifted upward. The R-R interval decreased more markedly during normocapnic hypoxia than normoxic hypercapnia and the arterial baroreflex sensitivity was decreased only by hypoxia. Cardiovascular responses to hypoxia were not affected by different levels of et-CO2. We conclude that concomitant hypoxia and hypercapnia, while increasing ventilation synergistically, exert an additive effect on cerebral blood flow. Increased sympathetic activity (and reduced baroreflex sensitivity) is one of the mechanisms by which hypoxia stimulates cardiac sympathetic activity.
KW - Baroreflex
KW - Cerebral circulation
KW - Chemoreflex
KW - Hypercapnia
KW - Hypoxia
UR - http://www.scopus.com/inward/record.url?scp=29144432076&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=29144432076&partnerID=8YFLogxK
U2 - 10.1007/s10286-005-0284-5
DO - 10.1007/s10286-005-0284-5
M3 - Article
C2 - 16362539
AN - SCOPUS:29144432076
VL - 15
SP - 373
EP - 381
JO - Clinical Autonomic Research
JF - Clinical Autonomic Research
SN - 0959-9851
IS - 6
ER -