Posthyperventilatory steal response in chronic cerebral hemodynamic stress: a positron emission tomography study.
OBJECTIVE
The alteration of regional cerebral blood flow (CBF) during and after hyperventilation was measured using positron emission tomography (PET) to determine the circulatory response induced by daily respiratory changes in the cerebral area under chronic hemodynamic stress.


METHODS
Three normal volunteers and 12 patients with an obstruction of major cerebral arteries underwent PET measurements of the CBF after an injection of H2(15)O: (1) in the resting condition, (2) during hyperventilation (HV scan), (3) 1 to 3 minutes after hyperventilation (post-HV scan), (4) during the inhalation of 5% CO2, and (5) after an injection of acetazolamide. Eleven patients also underwent a 15O gas study to measure CBF, oxygen extraction fraction (OEF), and cerebral blood volume (CBV).


RESULTS
(1) In 9 patients, the CBF value in the post-HV scan was lower than that in the HV scan in 1 or more regions in the area of the obstructed arteries, although the PaCO2 level during the post-HV scan was higher than that during the HV scan in all patients. All control regions in the patients and in the normal volunteers showed an elevated CBF in the post-HV scan compared with the HV scan. (2) The negative post-HV response (posthyperventilatory steal) was prominent in 4 patients with moyamoya vessels and in another 5 patients with atherosclerotic disease who had PET evidence of hemodynamic stress (elevated CBV or OEF). (3) The regional pre- to post-HV change in CBF was significantly correlated with the CBF responses to acetazolamide and CO2.


CONCLUSIONS
Vasodilatation after the termination of hyperventilation in the normal areas induces a steal response in the cerebral area suffering from hemodynamic stress and may cause profound hypoperfusion in everyday situations. This phenomenon may be important to our understanding of the clinical symptoms and the natural course of chronic cerebral occlusive disease bearing hemodynamic stress.
Nariai
T
T
Department of Neurosurgery, School of Medicine, Tokyo Medical and Dental University, and the Positron Medical Center, Japan. nariai.nsrg@med.tmd.ac.jp
Senda
M
M
Ishii
K
K
Wakabayashi
S
S
Yokota
T
T
Toyama
H
H
Matsushima
Y
Y
Hirakawa
K
K
D000086:Acetazolamide; D000280:Administration, Inhalation; D000328:Adult; D000368:Aged; D001810:Blood Volume / Q000502:physiology; D001921:Brain / Q000000981:diagnostic imaging; D002545:Brain Ischemia / Q000000981:diagnostic imaging / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation / Q000502:physiology; D002561:Cerebrovascular Disorders / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D002908:Chronic Disease; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D006985:Hyperventilation / Q000150:complications / Q000000981:diagnostic imaging* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology; D013312:Stress, Physiological / Q000000981:diagnostic imaging / Q000503:physiopathology*; D014055:Tomography, Emission-Computed
D002245:Carbon Dioxide; D000086:Acetazolamide