Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia

Peizhen Zhang, Xiangrong Shi, H. Fred Downey

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Abstract

The effect of moderately extended, intermittent-hypoxia (IH) on cerebral perfusion during changes in CO2was unknown. Thus, we assessed the changes in cerebral vascular conductance (CVC) and cerebral tissue oxygenation (ScO2) during experimental hypocapnia and hypercapnia following 14-day normobaric exposures to IH (10% O2). CVC was estimated from the ratio of mean middle cerebral arterial blood flow velocity (transcranial Doppler sonography) to mean arterial pressure (tonometry), and ScO2in the prefrontal cortex was monitored by near-infrared spectroscopy. Changes in CVC and ScO2during changes in partial pressure of end-tidal CO2(PETCO2, mass spectrometry) induced by 30-s paced-hyperventilation (hypocapnia) and during 6-min CO2rebreathing (hypercapnia) were compared before and after 14-day IH exposures in eight young nonsmokers. Repetitive IH exposures reduced the ratio of %ΔCVC/ΔPETCO2during hypocapnia (1.00 ± 0.13 vs 1.94 ± 0.35 vs %/mmHg, P = 0.026) and the slope of ΔCVC/ΔPETCO2during hypercapnia (1.79 ± 0.37 vs 2.97 ± 0.64 %/mmHg, P = 0.021), but had no significant effect on ΔScO2/ΔPETCO2. The ventilatory response to hypercapnia during CO2rebreathing was significantly diminished following 14-day IH exposures (0.83 ± 0.07 vs 1.14 ± 0.09 L/min/mmHg, P = 0.009). We conclude that repetitive normobaric IH exposures significantly diminish variations of cerebral perfusion in response to hypercapnia and hypocapnia without compromising cerebral tissue oxygenation. This IH-induced blunting of cerebral vasoreactivity during CO2variations helps buffer excessive oscillations of cerebral underperfusion and overperfusion while sustaining cerebral O2homeostasis.

Original languageEnglish
Pages (from-to)961-968
Number of pages8
JournalExperimental Biology and Medicine
Volume240
Issue number7
DOIs
StatePublished - 14 Jul 2015

Fingerprint

Hypocapnia
Hyperventilation
Mass spectrometry
Mass Spectrometry
Perfusion
Blood Vessels
Oxygenation
Tissue
Ultrasonography
Near infrared spectroscopy
Cerebrovascular Circulation
Flow velocity
Partial pressure
Doppler Transcranial Ultrasonography
Buffers
Brain Hypoxia
Blood
Near-Infrared Spectroscopy
Blood Flow Velocity
Partial Pressure

Keywords

  • CO<inf>2</inf>variations
  • Cerebral tissue oxygenation
  • ventilatory response

Cite this

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title = "Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia",
abstract = "The effect of moderately extended, intermittent-hypoxia (IH) on cerebral perfusion during changes in CO2was unknown. Thus, we assessed the changes in cerebral vascular conductance (CVC) and cerebral tissue oxygenation (ScO2) during experimental hypocapnia and hypercapnia following 14-day normobaric exposures to IH (10{\%} O2). CVC was estimated from the ratio of mean middle cerebral arterial blood flow velocity (transcranial Doppler sonography) to mean arterial pressure (tonometry), and ScO2in the prefrontal cortex was monitored by near-infrared spectroscopy. Changes in CVC and ScO2during changes in partial pressure of end-tidal CO2(PETCO2, mass spectrometry) induced by 30-s paced-hyperventilation (hypocapnia) and during 6-min CO2rebreathing (hypercapnia) were compared before and after 14-day IH exposures in eight young nonsmokers. Repetitive IH exposures reduced the ratio of {\%}ΔCVC/ΔPETCO2during hypocapnia (1.00 ± 0.13 vs 1.94 ± 0.35 vs {\%}/mmHg, P = 0.026) and the slope of ΔCVC/ΔPETCO2during hypercapnia (1.79 ± 0.37 vs 2.97 ± 0.64 {\%}/mmHg, P = 0.021), but had no significant effect on ΔScO2/ΔPETCO2. The ventilatory response to hypercapnia during CO2rebreathing was significantly diminished following 14-day IH exposures (0.83 ± 0.07 vs 1.14 ± 0.09 L/min/mmHg, P = 0.009). We conclude that repetitive normobaric IH exposures significantly diminish variations of cerebral perfusion in response to hypercapnia and hypocapnia without compromising cerebral tissue oxygenation. This IH-induced blunting of cerebral vasoreactivity during CO2variations helps buffer excessive oscillations of cerebral underperfusion and overperfusion while sustaining cerebral O2homeostasis.",
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Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia. / Zhang, Peizhen; Shi, Xiangrong; Downey, H. Fred.

In: Experimental Biology and Medicine, Vol. 240, No. 7, 14.07.2015, p. 961-968.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Two-week normobaric intermittent-hypoxic exposures stabilize cerebral perfusion during hypocapnia and hypercapnia

AU - Zhang, Peizhen

AU - Shi, Xiangrong

AU - Downey, H. Fred

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N2 - The effect of moderately extended, intermittent-hypoxia (IH) on cerebral perfusion during changes in CO2was unknown. Thus, we assessed the changes in cerebral vascular conductance (CVC) and cerebral tissue oxygenation (ScO2) during experimental hypocapnia and hypercapnia following 14-day normobaric exposures to IH (10% O2). CVC was estimated from the ratio of mean middle cerebral arterial blood flow velocity (transcranial Doppler sonography) to mean arterial pressure (tonometry), and ScO2in the prefrontal cortex was monitored by near-infrared spectroscopy. Changes in CVC and ScO2during changes in partial pressure of end-tidal CO2(PETCO2, mass spectrometry) induced by 30-s paced-hyperventilation (hypocapnia) and during 6-min CO2rebreathing (hypercapnia) were compared before and after 14-day IH exposures in eight young nonsmokers. Repetitive IH exposures reduced the ratio of %ΔCVC/ΔPETCO2during hypocapnia (1.00 ± 0.13 vs 1.94 ± 0.35 vs %/mmHg, P = 0.026) and the slope of ΔCVC/ΔPETCO2during hypercapnia (1.79 ± 0.37 vs 2.97 ± 0.64 %/mmHg, P = 0.021), but had no significant effect on ΔScO2/ΔPETCO2. The ventilatory response to hypercapnia during CO2rebreathing was significantly diminished following 14-day IH exposures (0.83 ± 0.07 vs 1.14 ± 0.09 L/min/mmHg, P = 0.009). We conclude that repetitive normobaric IH exposures significantly diminish variations of cerebral perfusion in response to hypercapnia and hypocapnia without compromising cerebral tissue oxygenation. This IH-induced blunting of cerebral vasoreactivity during CO2variations helps buffer excessive oscillations of cerebral underperfusion and overperfusion while sustaining cerebral O2homeostasis.

AB - The effect of moderately extended, intermittent-hypoxia (IH) on cerebral perfusion during changes in CO2was unknown. Thus, we assessed the changes in cerebral vascular conductance (CVC) and cerebral tissue oxygenation (ScO2) during experimental hypocapnia and hypercapnia following 14-day normobaric exposures to IH (10% O2). CVC was estimated from the ratio of mean middle cerebral arterial blood flow velocity (transcranial Doppler sonography) to mean arterial pressure (tonometry), and ScO2in the prefrontal cortex was monitored by near-infrared spectroscopy. Changes in CVC and ScO2during changes in partial pressure of end-tidal CO2(PETCO2, mass spectrometry) induced by 30-s paced-hyperventilation (hypocapnia) and during 6-min CO2rebreathing (hypercapnia) were compared before and after 14-day IH exposures in eight young nonsmokers. Repetitive IH exposures reduced the ratio of %ΔCVC/ΔPETCO2during hypocapnia (1.00 ± 0.13 vs 1.94 ± 0.35 vs %/mmHg, P = 0.026) and the slope of ΔCVC/ΔPETCO2during hypercapnia (1.79 ± 0.37 vs 2.97 ± 0.64 %/mmHg, P = 0.021), but had no significant effect on ΔScO2/ΔPETCO2. The ventilatory response to hypercapnia during CO2rebreathing was significantly diminished following 14-day IH exposures (0.83 ± 0.07 vs 1.14 ± 0.09 L/min/mmHg, P = 0.009). We conclude that repetitive normobaric IH exposures significantly diminish variations of cerebral perfusion in response to hypercapnia and hypocapnia without compromising cerebral tissue oxygenation. This IH-induced blunting of cerebral vasoreactivity during CO2variations helps buffer excessive oscillations of cerebral underperfusion and overperfusion while sustaining cerebral O2homeostasis.

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KW - ventilatory response

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