Mechanism and pattern of human cerebrovascular regulation after rapid changes in blood CO2 tension.

Shapiro, William; Wasserman, Alan G.; Patterson, John L.

doi:10.1172/jci105406

Cited by 52 publications

(36 citation statements)

References 23 publications

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“…In our study, the initial changes in CBF were observed in < 30 seconds; however, the time to achieve steadystate CBF was on the order of 1 to 2 minutes. These time scales are consistent with previous reports (Poulin et al, 1996;Shapiro et al, 1965Shapiro et al, , 1966.…”

Section: Discussionsupporting

confidence: 93%

Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

Jain

Langham

Floyd

et al. 2011

J Cereb Blood Flow Metab

100

144

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The effect of hypercapnia on cerebral metabolic rate of oxygen consumption (CMRO 2 ) has been a subject of intensive investigation and debate. Most applications of hypercapnia are based on the assumption that a mild increase in partial pressure of carbon dioxide has negligible effect on cerebral metabolism. In this study, we sought to further investigate the vascular and metabolic effects of hypercapnia by simultaneously measuring global venous oxygen saturation (S v O 2 ) and total cerebral blood flow (tCBF), with a temporal resolution of 30 seconds using magnetic resonance susceptometry and phase-contrast techniques in 10 healthy awake adults. While significant increases in S v O 2 and tCBF were observed during hypercapnia (P < 0.005), no change in CMRO 2 was noted (P > 0.05). Additionally, fractional changes in tCBF and end-tidal carbon dioxide (R 2 = 0.72, P < 0.005), as well as baseline S v O 2 and tCBF (R 2 = 0.72, P < 0.005), were found to be correlated. The data also suggested a correlation between cerebral vascular reactivity (CVR) and baseline tCBF (R 2 = 0.44, P = 0.052). A CVR value of 6.1% ± 1.6%/mm Hg was determined using a linear-fit model. Additionally, an average undershoot of 6.7%±4% and 17.1%±7% was observed in S v O 2 and tCBF upon recovery from hypercapnia in six subjects.

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Section: Discussionsupporting

confidence: 93%

Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

Jain

Langham

Floyd

et al. 2011

J Cereb Blood Flow Metab

100

144

View full text Add to dashboard Cite

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“…Hypercapnia and hypoxia are considered to cause decreased cerebrovascular resistance because of their effect on cerebral arteriolar tone (6,10,22). The effect of hyperoxia and hypercapnia on carotid artery blood flow has been reported to be variable (2), and our findings are similar to a previous report (12) that found no significant effect of hypercapnia on carotid artery flow, although middle cerebral artery flow was increased.…”

Section: Discussionsupporting

confidence: 89%

Measurement of hemodynamics in human carotid artery using ultrasound and computational fluid dynamics

Starmans-Kool

Stanton

Zhao

et al. 2002

Journal of Applied Physiology

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Measurement of hemodynamics in human carotid artery using ultrasound and computational fluid dynamics. J Appl Physiol 92: 957-961, 2002; 10.1152/japplphysiol.00171.2001.-The objective of the study was to investigate the feasibility of using computational fluid dynamic modeling (CFD) with noninvasive ultrasound measurements to determine time-variant three-dimensional (3D) carotid arterial hemodynamics in humans in vivo. The effects of hyperoxia and hypoxic hypercapnia on carotid artery local hemodynamics were examined by use of this approach. Six normotensive volunteers followed a double-blind randomized crossover design. Blood pressure, heart rate, and carotid blood flow were measured while subjects breathed normal air, a mixture of 5% CO2 and 15% O2 (hypoxic hypercapnia), and 100% O2 (hyperoxia). Carotid artery geometry was reconstructed on the basis of B-mode ultrasound images by using purpose-built image processing software. Time-variant 3D carotid hemodynamics were estimated by using finite volume-based CFD. Systemic blood pressure was not significantly affected by hyperoxia or hypoxic hypercapnia, but heart rate decreased significantly with hyperoxia. There was an increase in diastolic flow velocity in the external carotid artery after hypoxic hypercapnia, but otherwise carotid blood flow velocities did not change significantly. Compared with normal air, hyperoxic conditions were associated with a decrease in the width of the region of flow separation in the external carotid artery. During hyperoxia, there was also an increase in the minimum and a decrease in maximum shear stress in the bifurcation and hence a reduction in cyclic variation in shear stress. Hypoxic hypercapnia was associated with a reduced duration of flow separation in the external carotid artery and an increase in the minimum shear stress without affecting the cyclic variation in shear stress. This study demonstrates the feasibility of using noninvasive ultrasound techniques in conjunction with CFD to describe time-variant 3D hemodynamics in the human carotid arterial bifurcation in vivo. blood flow; hyperoxia; hypoxic hypercapnia; shear stress ATHEROSCLEROSIS IS A MAJOR cause of cardiovascular mortality and morbidity. An important feature of atherosclerosis is the focal nature of lesions and their characteristic location at particular sites in the vasculature, such as regions of marked curvature and branch points (24, 28). It has been proposed that this is a consequence of local hemodynamics in such regions (4) and that shear stress gradients adversely affect endothelial function at such sites (8, 9) and, hence, increase the risk of atheroma formation (11, 23). However, the measurement of flow and shear stress in the regions relevant to atheroma formation (e.g., arterial bifurcations) is difficult because of the complex nature of flows at such sites. Computational flow dynamic modeling (CFD) is widely used in engineering to calculate flows in complex geometries, and recently this approach has been successfully applied to modeling flow in ...

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“…This incorporates calculating cerebrovascular changes during rapid changes in ETCO 2 . In addition, Shapiro et al 12 reported on the presence of hysteresis due to the delayed response of CBFV to a step change in PCO 2 . Hence, for each artery the time delay was estimated by the cross-correlation function peak position between CBFV and ETCO 2 .…”

Section: Methodsmentioning

confidence: 99%

Can Cerebrovascular Reactivity Be Assessed Without Measuring Blood Pressure in Patients With Carotid Artery Disease?

Dumville

Panerai

Lennard

et al. 1998

Stroke

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Background and Purpose-Conventional methods of assessing cerebrovascular reactivity (CVR) omit the influence of blood pressure (BP). This study demonstrates the significant influence of BP during the assessment of CVR in patients with carotid artery disease. Methods-In 56 subjects the CVR was bilaterally assessed by measurement of cerebral blood flow velocity change in response to inhalation of 5% CO 2 in air while BP was continuously monitored. Three methods of calculating the CVR were used: the conventional ratio between relative cerebral blood flow velocity and end-tidal CO 2 , simple linear regression, and multiple linear regression analysis (MLRA). The clinical significance of the difference in CVR indices was evaluated. The Bland-Altman test was applied to quantify the comparability and bias between measurements. The magnitude and significance of a change in BP during the CVR assessment were calculated in conjunction with an estimate of the velocity change attributed to the BP. The statistical significance of the data segment length on the variability and magnitude of the CVR index was computed. Results-The value of the CVR index was reduced by 20% and 6% in comparison to the conventional ratio approach when MLRA and linear regression were applied, respectively. With the use of MLRA, in 96% of cases the value of the BP coefficient was statistically significant, and in four patients the increase in velocity was primarily attributed to the increase in BP. Conclusions-The influence of BP is significant and requires consideration when the CVR index is calculated in patients with carotid artery disease. (Stroke. 1998;29:968-974.)

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Mechanism and pattern of human cerebrovascular regulation after rapid changes in blood CO2 tension.

Cited by 52 publications

References 23 publications

Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

Measurement of hemodynamics in human carotid artery using ultrasound and computational fluid dynamics

Can Cerebrovascular Reactivity Be Assessed Without Measuring Blood Pressure in Patients With Carotid Artery Disease?

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