Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea

Krzysztof Narkiewicz, Philippe J H Van De Borne, Catherine A. Pesek, Mark E. Dyken, Nicola Montano, Virend Somers

Research output: Contribution to journalArticle

387 Citations (Scopus)

Abstract

Background - The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. Methods and Results - We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43±4 versus 21±3 bursts per minute; P<0.001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8±0.8 versus 3.2±0.7 L/min; P=0.02), heart rate (10±1 versus 7±1 bpm; P=0.03), and mean arterial pressure (7±2 versus 0±2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106±20%)was greater than in control subjects (52±23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24±6%) than in control subjects (7±5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects. Conclusions - OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.

Original languageEnglish (US)
Pages (from-to)1183-1189
Number of pages7
JournalCirculation
Volume99
Issue number9
StatePublished - Mar 9 1999
Externally publishedYes

Fingerprint

Obstructive Sleep Apnea
Hypercapnia
Apnea
Muscles
Ventilation
Respiration
Heart Rate
Blood Pressure
Hypoxia
Arterial Pressure
Body Mass Index
Hemodynamics
Hypertension

Keywords

  • Blood pressure
  • Heart rate
  • Hypoxia
  • Nervous system
  • Sleep

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Narkiewicz, K., Van De Borne, P. J. H., Pesek, C. A., Dyken, M. E., Montano, N., & Somers, V. (1999). Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea. Circulation, 99(9), 1183-1189.

Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea. / Narkiewicz, Krzysztof; Van De Borne, Philippe J H; Pesek, Catherine A.; Dyken, Mark E.; Montano, Nicola; Somers, Virend.

In: Circulation, Vol. 99, No. 9, 09.03.1999, p. 1183-1189.

Research output: Contribution to journalArticle

Narkiewicz, K, Van De Borne, PJH, Pesek, CA, Dyken, ME, Montano, N & Somers, V 1999, 'Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea', Circulation, vol. 99, no. 9, pp. 1183-1189.
Narkiewicz K, Van De Borne PJH, Pesek CA, Dyken ME, Montano N, Somers V. Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea. Circulation. 1999 Mar 9;99(9):1183-1189.
Narkiewicz, Krzysztof ; Van De Borne, Philippe J H ; Pesek, Catherine A. ; Dyken, Mark E. ; Montano, Nicola ; Somers, Virend. / Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea. In: Circulation. 1999 ; Vol. 99, No. 9. pp. 1183-1189.
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abstract = "Background - The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. Methods and Results - We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43±4 versus 21±3 bursts per minute; P<0.001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8±0.8 versus 3.2±0.7 L/min; P=0.02), heart rate (10±1 versus 7±1 bpm; P=0.03), and mean arterial pressure (7±2 versus 0±2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106±20{\%})was greater than in control subjects (52±23{\%}; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24±6{\%}) than in control subjects (7±5{\%}) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects. Conclusions - OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.",
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AU - Montano, Nicola

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N2 - Background - The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. Methods and Results - We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43±4 versus 21±3 bursts per minute; P<0.001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8±0.8 versus 3.2±0.7 L/min; P=0.02), heart rate (10±1 versus 7±1 bpm; P=0.03), and mean arterial pressure (7±2 versus 0±2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106±20%)was greater than in control subjects (52±23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24±6%) than in control subjects (7±5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects. Conclusions - OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.

AB - Background - The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. Methods and Results - We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43±4 versus 21±3 bursts per minute; P<0.001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8±0.8 versus 3.2±0.7 L/min; P=0.02), heart rate (10±1 versus 7±1 bpm; P=0.03), and mean arterial pressure (7±2 versus 0±2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106±20%)was greater than in control subjects (52±23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24±6%) than in control subjects (7±5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects. Conclusions - OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.

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