title: Reactivity of cerebral blood flow to carbon dioxide in hypertensive patients: evaluation by the transcranial Doppler method.
abstract: OBJECTIVE
  To evaluate hypertensive cerebral involvement before cerebrovascular accidents.
  
  
  METHODS
  Cerebral microvascular responses to changes in the arterial partial pressure of CO2 (pCO2; the CO2 reactivity) were compared among patients with different stages and severity of hypertensive disease.
  
  
  METHODS
  Fifty-eight patients with hypertension, 11 with borderline hypertension, 15 hypertensives with cerebral infarction and 58 normotensive controls were studied.
  
  
  METHODS
  The cerebrovascular CO2 reactivity was determined by measuring simultaneously the end-tidal pCO2 and the blood flow velocity in the middle cerebral artery using transcranial Doppler sonography under hypocapnic, normocapnic and hypercapnic conditions.
  
  
  RESULTS
  CO2 reactivity was impaired in the hypertensive patients compared with in the normotensive controls, but less so than in the symptomatic hemisphere of the hypertensive patients with cerebral infarction. The CO2 reactivity in the borderline hypertensive patients was greater than that in both the symptomatic and asymptomatic hemispheres of the hypertensive patients with cerebral infarction. In the subjects without cerebral infarction, two risk factors for cerebral atherosclerosis (age and hypertension) were negatively correlated with cerebrovascular CO2 reactivity. In the hypertensive patients age and the estimated duration of hypertension were negatively correlated with cerebrovascular CO2 reactivity. CO2 reactivity in the patients with hypertensive or arteriosclerotic retinopathy or ST-T changes on their electrocardiogram was impaired compared with that in the patients without such changes.
  
  
  CONCLUSIONS
  Hypertension affected the microvascular reactivity of the brain before the development of cerebrovascular accidents, and its effect varied dependently on the extent of involvement of other target organs.
authors.affiliation: First Department of Internal Medicine, Osaka University Medical School, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Maeda
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
authors.forename: N
authors.initials: N
authors.lastname: Handa
authors.forename: H
authors.initials: H
authors.lastname: Hougaku
authors.forename: S
authors.initials: S
authors.lastname: Ogawa
authors.forename: T
authors.initials: T
authors.lastname: Itoh
authors.forename: Y
authors.initials: Y
authors.lastname: Tsukamoto
authors.forename: T
authors.initials: T
authors.lastname: Kamada
mesh_terms: D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000000981:diagnostic imaging / Q000209:etiology; D001783:Blood Flow Velocity / Q000502:physiology; D002245:Carbon Dioxide / Q000097:blood*; D002544:Cerebral Infarction / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000209:etiology; D005260:Female; D006801:Humans; D006935:Hypercapnia / Q000503:physiopathology; D006973:Hypertension / Q000097:blood / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016857:Hypocapnia / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D002245:Carbon Dioxide