Cerebral blood-flow responses to induced hypotension and to CO2 inhalationin patients with major cerebral artery occlusive disease: a positron-emission tomography study

Our aim was to study the relationship between cerebral blood flow (CBF) res ponses to induced hypotension and to CO2 inhalation in patients with occlus ive disease of the carotid or middle cerebral arteries. In 13 patients (8 m en, 5 women) aged 31-73 years (mean +/- 1 SD = 63.2 +/- 10.6), regional CBF values during the resting state (CBFrest), 7% CO2 inhalation (CBFhypercapn ia), and hypotension induced by 10-20 mu g/kg/min intravenous trimethaphan (CBFhypotension) were measured using positron-emission tomography (PET) wit h (H2O)-O-15. The % CBF change during induced hypotension (% CBFhypotension ) was defined as (CBFhypotension - - CBFrest)/CBFrest multiplied by 100. Th e % CBF change during CO2 inhalation (% CBFhypercapnia) was defined as (CBF hypercapnia - CBFrest)/CBFrest/mm Hg arterial partial pressure of CO2 x 100 . We defined symptomatic hemispheres as those with a stenotic or occlusive lesion with neurological symptoms or signs and asymptomatic hemispheres as those which had a similar lesion and/or were influenced by the collateral f low pattern without neurological symptoms. In the territory of the occlusiv e lesion, % CBFhypotension also correlated significantly with % CBFhypercap nia (r = 0.793, P < 0.002) in the symptomatic hemispheres. In the brain reg ions in which trimethaphan did not induce a reduction in CBF, % CBF,,,,,,,, ,;, was 6.13 +/- 1.79. In those in which % CBFhypotension ranged from 0 to -5, from -5 to -10, and more than -10%, % CBFhypercapnia was 4.05 +/- 1.99, 3.21 +/- 1.17, and 1.73 +- 1.61, respectively, with significant difference s between each pair of groups. In the asymptomatic hemispheres, % CBF also correlated with % CBFhypotension hypercapnia (r = 0.979, P < 0.0001). Failu re to maintain CBF during induced hypotension was associated with diminishe d cerebrovascular vasoreactivity to hypercapnia in patients with arterial d isease. This may indicate that failure of autoregulation can be assessed by the CBF response to both induced hypotension and CO2 inhalation. From the technical point of view, estimation of the CO2 response may be useful for a ssessing failure of autoregulation.