title: Effects of acute hypoxia on cerebrovascular responses to carbon dioxide.
abstract: In normoxic conditions, a reduction in arterial carbon dioxide tension causes cerebral vasoconstriction, thereby reducing cerebral blood flow and modifying dynamic cerebral autoregulation (dCA). It is unclear to what extent these effects are altered by acute hypoxia and the associated hypoxic ventilatory response (respiratory chemoreflex). This study tested the hypothesis that acute hypoxia attenuates arterial CO2 tension-mediated regulation of cerebral blood flow to help maintain cerebral O2 homeostasis. Eight subjects performed three randomly assigned respiratory interventions following a resting baseline period, as follows: (1) normoxia (21% O2); (2) hypoxia (12% O2); and (3) hypoxia with wilful restraint of the respiratory chemoreflex. During each intervention, 0, 2.0, 3.5 or 5.0% CO2 was sequentially added (8 min stages) to inspired gas mixtures to assess changes in steady-state cerebrovascular CO2 reactivity and dCA. During normoxia, the addition of CO2 increased internal carotid artery blood flow and middle cerebral artery mean blood velocity (MCA Vmean), while reducing dCA (change in phase = -0.73 ± 0.22 rad, P = 0.005). During acute hypoxia, internal carotid artery blood flow and MCA Vmean remained unchanged, but cerebrovascular CO2 reactivity (internal carotid artery, P = 0.003; MCA Vmean, P = 0.031) and CO2-mediated effects on dCA (P = 0.008) were attenuated. The effects of hypoxia were not further altered when the respiratory chemoreflex was restrained. These findings support the hypothesis that arterial CO2 tension-mediated effects on the cerebral vasculature are reduced during acute hypoxia. These effects could limit the degree of hypocapnic vasoconstriction and may help to regulate cerebral blood flow and cerebral O2 homeostasis during acute periods of hypoxia.
authors.affiliation: Department of Biomedical Engineering, Toyo University, Kawagoe-Shi, Saitama, Japan ogoh@toyo.jp.
authors.forename: Shigehiko
authors.initials: S
authors.lastname: Ogoh
authors.affiliation: Morinomiya University of Medical Sciences, Osaka, Japan.
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Nakahara
authors.affiliation: Morinomiya University of Medical Sciences, Osaka, Japan.
authors.forename: Shinya
authors.initials: S
authors.lastname: Ueda
authors.affiliation: Department of Environmental Physiology for Exercise, Osaka City University Graduate School of Medicine, Osaka, Japan.
authors.forename: Kazunobu
authors.initials: K
authors.lastname: Okazaki
authors.affiliation: Department of Environmental Health, Nara Women's University, Nara, Japan.
authors.forename: Manabu
authors.initials: M
authors.lastname: Shibasaki
authors.affiliation: Department of Biology, University of Colorado, Colorado Springs, CO, USA.
authors.forename: Andrew W
authors.initials: AW
authors.lastname: Subudhi
authors.affiliation: Morinomiya University of Medical Sciences, Osaka, Japan Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.
authors.forename: Tadayoshi
authors.initials: T
authors.lastname: Miyamoto
mesh_terms: D000328:Adult; D001783:Blood Flow Velocity / Q000502:physiology; D002245:Carbon Dioxide / Q000008:administration & dosage* / Q000097:blood*; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D000860:Hypoxia / Q000097:blood* / Q000503:physiopathology; D008297:Male; D013997:Time Factors; D055815:Young Adult
chemical_list: D002245:Carbon Dioxide