Key result
Hypertension is not associated with differences in cerebrovascular CO2 reactivity compared to normotension.
Observational (n=16)
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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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Tominaga et al. (1976) conducted an observational in Hypertension (n=16). Hypertension (during CO2 inhalation and voluntary hyperventilation) vs. Normotension was evaluated on Cerebrovascular reactivity (cerebral blood flow calculated as initial slope index via intracarotid 133Xe clearance). Hypertensive and normotensive patients showed no difference in CO2 cerebrovascular reactivity, averaging 6±2% above PaCO2 35 mm Hg and ~2% below 30 mm Hg.
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