Regional Differences in Cerebral Vascular Response to P_aco₂ Changes in Humans Measured by Positron Emission Tomography

Abstract

Hypercapnia and hypocapnia produce cerebral vasodilation and vasoconstriction, respectively. However, regional differences in the vascular response to changes in Paco2 in the human brain are not pronounced. In the current study, these regional differences were evaluated. In each of the 11 healthy subjects, cerebral blood flow (CBF) was measured using 15O-water and positron emission tomography at rest and during hypercapnia and hypocapnia. All CBF images were globally normalized for CBF and transformed into the standard brain anatomy. t values between rest and hypercapnia or hypocapnia conditions were calculated on a pixel-by-pixel basis. In the pons, cerebellum, thalamus, and putamen, significant relative hyperperfusion during hypercapnia was observed, indicating a large capacity for vasodilatation. In the pons and putamen, a significant relative hypoperfusion during hypocapnia, that is, a large capacity for vasoconstriction, was also observed, indicating marked vascular responsiveness. In the temporal, temporo-occipital, and occipital cortices, significant relative hypoperfusion during hypercapnia and significant relative hypoperfusion during hypocapnia were observed, indicating that cerebral vascular tone at rest might incline toward vasodilatation. Such regional heterogeneity of the cerebral vascular response should be considered in the assessment of cerebral perfusion reserve by hypercapnia and in the correction of CBF measurements for variations in subjects' resting Paco2.

Imaging incorporation of circulating docosahexaenoic acid into the human brain using positron emission tomography

“…Our PVE-corrected (and uncorrected) values for rCBF were comparable to values reported in other studies; mean gray matter PVE-uncorrected V b (0.057 6 0.008 ml/ml) was similar to the mean reported in a prior PET ARA study (0.055 6 0.006 ml/ml) (35,36,60 Regional values of K* for DHA were significantly correlated with rCBF in 12 of the 14 subjects. This correlation was not determined by a dependence of K* on rCBF but by the fact that both parameters represent common aspects of regional brain metabolism.…”

Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

“…33 Animal and human studies have both demonstrated significant CBF increases in response to hypercapnia. [5][6][7]12,13,[16][17][18][33][34][35][36][37][38][39] This reaction has been exploited with tests such as the hypercapnia challenge to evaluate cerebrovascular reserve. 2,7,8 Previous human studies demonstrated up to a 200% increase in CBF as pCO 2 was raised experimentally.…”

“…4,7,[11][12][13][14][15][16][17][18][19][20][21][22] Most experimental studies of hypercapnia increase pCO 2 through rebreathing techniques or 5% CO 2 air mixtures. These methods result in a mild increase in pCO 2 of approximately 5 to 8 mm Hg.…”

“…3,4,[7][8][9][10][11][12][13] Techniques such as transcranial Doppler, nuclear medicine positronemission tomography (PET) and single-photon emission CT, angiography, phase-contrast MR imaging, and arterial spinlabeled (ASL) MR perfusion have been used to evaluate the experimental hypercapnic effect on cerebral perfusion. 4,7,[11][12][13][14][15][16][17][18][19][20][21][22][23] It is not uncommon that hospitalized patients can have marked increases in pCO 2 in excess of 30 mm Hg from baseline, both on an acute or on a chronic basis. In a similar fashion, hyperventilation may produce marked hypocapnia.…”

Changes in Human Cerebral Blood Flow and Cerebral Blood Volume during Hypercapnia and Hypocapnia Measured by Positron Emission Tomography

“…Hypercapnia induces cerebral vasodilation and increases cerebral blood flow (CBF), and hypocapnia induces cerebral vasoconstriction and decreases CBF (Kety and Schmidt, 1948;Raper et al, 1971;Ito et al, 2000). Because the vascular responsiveness to vasodilator in the brain with insufficient cerebral perfusion pressure is reduced by autoregulatory vasodilation , hypercapnia can be used to estimate cerebral perfusion reserve in occlusive cerebrovascular disease (Herold et al, 1988;Levine et al, 1991;Kuwabara et al, 1997).…”