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
N1 - Funding Information:
We sincerely thank our volunteer subjects for their cheerful cooperation. This study was supported in part by the University of North Texas Health Science Center Foundation and by a Government Scholarship from People’s Republic of China to Dr. Peizhen Zhang.
Publisher Copyright:
© 2014, © 2014 by the Society for Experimental Biology and Medicine.
PY - 2015/7/14
Y1 - 2015/7/14
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.
KW - COvariations
KW - Cerebral tissue oxygenation
KW - ventilatory response
UR - http://www.scopus.com/inward/record.url?scp=84936934478&partnerID=8YFLogxK
U2 - 10.1177/1535370214562339
DO - 10.1177/1535370214562339
M3 - Article
C2 - 25504012
AN - SCOPUS:84936934478
SN - 1535-3702
VL - 240
SP - 961
EP - 968
JO - Experimental Biology and Medicine
JF - Experimental Biology and Medicine
IS - 7
ER -