Stroke, Vol 7, 507-510, Copyright © 1976 by American Heart Association
S Tominaga, S Strandgaard, K Uemura, K Ito and T Kutsuzawa
Cerebrovascular reactivity to CO2 inhalation and voluntary hyperventilation
was studied in seven normotensive subjects and nine hypertensive patients
without clinical or angiographical signs of arteriosclerosis. Cerebral
blood flow (CBF) was measured by the intracarotid 133Xe clearance method
and calculated as the initial slope index. Three to five CBF measurements
were made in each patient in the PaCO2 range of 20 to 55 mm Hg. No
difference was observed in reactivity between hypertensive and normotensive
patients, either during CO2 inhalation or during hyperventilation. The
shape of the CBF:PaCO2 curve suggested a decrease in reactivity below a
PaCO2 of 30 to 35 mm Hg in both groups. Above a PaCO2 of 35 mm Hg,
exponential regression analysis yielded a mean reactivity of 6 +/- 2%,
whereas below a PaCO2 of 30 mm Hg it was about 2%. The rise in CBF during
CO2 inhalation was not influenced by the intravenous infusion of a small
dose of trimethaphan which blocked the concomitant rise in blood pressure.
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Cerebrovascular CO2 reactivity in normotensive and hypertensive man
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