Analysis of dynamic cerebral autoregulation using an ARX model based on arterial blood pressure and middle cerebral artery velocity simulation

2002 ◽  
Vol 40 (5) ◽  
pp. 600-605 ◽  
Author(s):  
Y. Liu ◽  
R. Allen
Keyword(s):  
Blood Pressure ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Cerebral Autoregulation ◽  
Arx Model ◽  
Model Based ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

Effect of inhibition of nitric oxide synthase on dynamic cerebral autoregulation in humans

2000 ◽  
Vol 99 (6) ◽  
pp. 555-560 ◽  
Author(s):  
R. P. WHITE ◽  
P. VALLANCE ◽  
H. S. MARKUS
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Cerebral Autoregulation ◽  
Arterial Blood ◽  
The Mean ◽  
Oxide Synthase ◽  
Dynamic Cerebral Autoregulation

Cerebral blood flow is maintained constant over a range of cerebral perfusion pressures by cerebral autoregulation. Impaired cerebral autoregulation may be important in the pathogenesis of cerebral ischaemia. The mechanisms mediating normal cerebral autoregulation in humans are poorly understood. We used a recently described transcranial Doppler technique, which allows non-invasive measurement of dynamic cerebral autoregulation, to test the hypothesis that nitric oxide mediates cerebral autoregulation. The rate of rise of middle cerebral artery blood flow velocity, compared with that of arterial blood pressure, was determined following a stepwise fall in arterial blood pressure, in order to calculate an autoregulatory index. The effect of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) on dynamic autoregulation was compared with that of noradrenaline titrated to result in a similar rise in blood pressure. Six healthy subjects were studied in each group. The mean (S.D.) change in autoregulatory index following noradrenaline at a similar pressor dose was significantly greater than the change following the L-NMMA bolus: 1.1 (1.2) compared with -0.8 (0.8) for the left middle cerebral artery (P = 0.002), and 1.1 (0.8) compared with -0.8 (0.8) for the right middle cerebral artery (P = 0.002). There was no difference in the mean (S.D.) blood pressure increase resulting from the two agents: L-NMMA, 19.7 (7.4) mmHg; noradrenaline, 15.5 (4.8) mmHg (P = 0.281). These results suggest that nitric oxide mediates at least part of the dynamic phase of cerebral autoregulation in humans. Reduced nitric oxide release may play a role in the impaired cerebral autoregulation seen in patients with, or at risk of, cerebral ischaemia.

Impaired cerebrovascular autoregulation and reduced CO2 reactivity after long duration spaceflight

2012 ◽  
Vol 302 (12) ◽  
pp. H2592-H2598 ◽  
Author(s):  
K. A. Zuj ◽  
Ph. Arbeille ◽  
J. K. Shoemaker ◽  
A. P. Blaber ◽  
D. K. Greaves ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Resistance Index ◽  
Arma Model ◽  
Functional Changes ◽  
Cerebrovascular Autoregulation ◽  
Arterial Blood ◽  
Long Duration

Long duration habitation on the International Space Station (ISS) is associated with chronic elevations in arterial blood pressure in the brain compared with normal upright posture on Earth and elevated inspired CO2. Although results from short-duration spaceflights suggested possibly improved cerebrovascular autoregulation, animal models provided evidence of structural and functional changes in cerebral vessels that might negatively impact autoregulation with longer periods in microgravity. Seven astronauts (1 woman) spent 147 ± 49 days on ISS. Preflight testing (30–60 days before launch) was compared with postflight testing on landing day ( n = 4) or the morning 1 ( n = 2) or 2 days ( n = 1) after return to Earth. Arterial blood pressure at the level of the middle cerebral artery (BPMCA) and expired CO2 were monitored along with transcranial Doppler ultrasound assessment of middle cerebral artery (MCA) blood flow velocity (CBFV). Cerebrovascular resistance index was calculated as (CVRi = BPMCA/CBFV). Cerebrovascular autoregulation and CO2 reactivity were assessed in a supine position from an autoregressive moving average (ARMA) model of data obtained during a test where two breaths of 10% CO2 were given four times during a 5-min period. CBFV and Doppler pulsatility index were reduced during −20 mmHg lower body negative pressure, with no differences pre- to postflight. The postflight indicator of dynamic autoregulation from the ARMA model revealed reduced gain for the CVRi response to BPMCA ( P = 0.017). The postflight responses to CO2 were reduced for CBFV ( P = 0.056) and CVRi ( P = 0.047). These results indicate that long duration missions on the ISS impaired dynamic cerebrovascular autoregulation and reduced cerebrovascular CO2 reactivity.

scholarly journals Larger Anastomoses in Angiotensinogen-Knockout Mice Attenuate Early Metabolic Disturbances after Middle Cerebral Artery Occlusion

1999 ◽  
Vol 19 (10) ◽  
pp. 1092-1098 ◽  
Author(s):  
Keiichiro Maeda ◽  
Ryuji Hata ◽  
Michael Bader ◽  
Thomas Walther ◽  
Konstantin-Alexander Hossmann
Keyword(s):  
Blood Pressure ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Knockout Mice ◽  
Therapeutic Window ◽  
Wild Type ◽  
Arterial Blood ◽  
Mca Occlusion

Abnormalities in the homeostasis of the renin-angiotensin system have been implicated in the pathogenesis of vascular disorders, including stroke. The authors investigated whether angiotensinogen (AGN) knockout mice exhibit differences in brain susceptibility to focal ischemia, and whether such differences can be related to special features of the collateral circulation. Wild-type and AGN-knockout mice were submitted to permanent suture occlusion of the middle cerebral artery (MCA). The collateral vascular system was visualized by systemic latex infusion, and the ischemic lesions were identified by cresyl-violet staining. The core and penumbra of the evolving infarct were differentiated by bioluminescence and autoradiographic imaging of A TP and protein biosynthesis, respectively. In wild-type mice, mean arterial blood pressure was 95.0 ± 8.6 mm Hg, and the diameter of fully relaxed anastomotic vessels between the peripheral branches of the anterior and middle cerebral arteries 26.6 ± 4.0 μm In AGN knockouts, mean arterial blood pressure was significantly lower, 71.5 ± 8.5 mm Hg ( P <,01), and the anastomotic vessels were significantly larger, 29.4 ± 4.6 μm ( P < .01). One hour after MCA occlusion, AGN-knockout mice exhibited a smaller ischemic core (defined as the region of ATP depletion) but a larger penumbra (the area of disturbed protein synthesis with preserved ATP). At 24 hours after MCA occlusion, this difference disappeared, and histologically visible lesions were of similar size in both strains. The observations show that in AGN-knockout mice the more efficient collateral blood supply delays ischemic injury despite the lower blood pressure. Pharmacologic suppression of angiotensin formation may prolong the therapeutic window for treatment of infarcts.

The Impact of Systemic Vasoconstrictors on the Cerebral Circulation of Anesthetized Patients 

1998 ◽  
Vol 89 (1) ◽  
pp. 67-72 ◽  
Author(s):  
Stephan P. Strebel ◽  
Christoph Kindler ◽  
Bruno Bissonnette ◽  
Gabriela Tschaler ◽  
Dubravka Deanovic
Keyword(s):  
Blood Pressure ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Cerebral Circulation ◽  
Internal Carotid ◽  
Arterial Blood

Unlabelled BACKGROUND. The effect of vasoconstrictors on intracerebral hemodynamics in anesthetized patients is controversial. The influence of phenylephrine and norepinephrine on the cerebral circulation was investigated in isoflurane- or propofol-anesthetized patients using transcranial Doppler ultrasonography. Methods Forty patients were randomly assigned to have vasoconstrictor tests with norepinephrine or phenylephrine during either isoflurane or propofol anesthesia. Blood flow velocities were simultaneously measured in the middle cerebral artery and ipsilateral extracranial internal carotid artery. Baseline recordings were done during stable anesthesia in a supine position (test 0). A second series of measurements were performed after norepinephrine or phenylephrine had increased mean arterial blood pressure by about 20% (test 1). With maintained norepinephrine or phenylephrine infusion, a final series of results were obtained after the increased mean arterial blood pressure was counteracted by a slightly head-up patient position (test 2). Results Both vasoconstrictors significantly increased mean flow velocities in the middle cerebral artery (norepinephrine: 43 +/- 11 cm/s to 49 +/- 11 cm/s; phenylephrine: 43 +/- 8 cm/s to 48 +/- 9 cm/s; +/- SD) and internal carotid artery (norepinephrine: 27 +/- 7 cm/s to 31 +/- 8 cm/s; phenylephrine: 27 +/- 9 cm/s to 31 +/- 10 cm/s) in the isoflurane-but not in the propofol-anesthetized patients. In the head-up position, only small and insignificant flow velocity changes were observed in both cerebral arteries independent of the vasoconstrictor or background anesthetic. Conclusions The results of the present study indicate that norepinephrine and phenylephrine do not directly affect intracranial hemodynamics in anesthetized patients, but rather that hemodynamic changes observed with vasoconstrictors reflect the effect of the background anesthetic agents on cerebral pressure autoregulation.

Random perturbations of arterial blood pressure for the assessment of dynamic cerebral autoregulation

2012 ◽  
Vol 33 (2) ◽  
pp. 103-116 ◽  
Author(s):  
Emmanuel Katsogridakis ◽  
Glen Bush ◽  
Lingke Fan ◽  
Anthony A Birch ◽  
David M Simpson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Random Perturbations ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

Cerebral blood flow responses to changes in oxygen and carbon dioxide in humans

2002 ◽  
Vol 80 (8) ◽  
pp. 819-827 ◽  
Author(s):  
Andrea Vovk ◽  
David A Cunningham ◽  
John M Kowalchuk ◽  
Donald H Paterson ◽  
James Duffin
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Middle Cerebral Artery ◽  
Arterial Blood Pressure ◽  
Cerebral Artery ◽  
Mean Arterial Blood Pressure ◽  
Transcranial Doppler Ultrasound ◽  
Arterial Blood ◽  
End Tidal

This study characterized cerebral blood flow (CBF) responses in the middle cerebral artery to PCO2ranging from 30 to 60 mmHg (1 mmHg = 133.322 Pa) during hypoxia (50 mmHg) and hyperoxia (200 mmHg). Eight subjects (25 ± 3 years) underwent modified Read rebreathing tests in a background of constant hypoxia or hyperoxia. Mean cerebral blood velocity was measured using a transcranial Doppler ultrasound. Ventilation (VE), end-tidal PCO2 (PETCO2), and mean arterial blood pressure (MAP) data were also collected. CBF increased with rising PETCO2 at two rates, 1.63 ± 0.21 and 2.75 ± 0.27 cm·s–1·mmHg–1 (p < 0.05) during hypoxic and 1.69 ± 0.17 and 2.80 ± 0.14 cm·s–1·mmHg–1 (p < 0.05) during hyperoxic rebreathing. VE also increased at two rates (5.08 ± 0.67 and 10.89 ± 2.55 L·min–1·mmHg–1 and 3.31 ± 0.50 and 7.86 ± 1.43 L·min–1·mmHg–1) during hypoxic and hyperoxic rebreathing. MAP and PETCO2 increased linearly during both hypoxic and hyperoxic rebreathing. The breakpoint separating the two-component rise in CBF (42.92 ± 1.29 and 49.00 ± 1.56 mmHg CO2 during hypoxic and hyperoxic rebreathing) was likely not due to PCO2 or perfusion pressure, since PETCO2 and MAP increased linearly, but it may be related to VE, since both CBF and VE exhibited similar responses, suggesting that the two responses may be regulated by a common neural linkage. Key words: brain blood flow, middle cerebral artery, ventilation, mean arterial blood pressure.

scholarly journals Differentiating Dynamic Cerebral Autoregulation Across Vascular Territories

2021 ◽  
Vol 12 ◽  
Author(s):  
Navpreet Reehal ◽  
Stephanie Cummings ◽  
Michael T. Mullen ◽  
Wesley B. Baker ◽  
David Kung ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Transcranial Doppler ◽  
Cerebral Autoregulation ◽  
Posterior Cerebral Artery ◽  
Function Analysis ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Dynamic Cerebral Autoregulation

Objective: Transcranial Doppler is commonly used to calculate cerebral autoregulation, but measurements are typically restricted to a single cerebral artery. In exploring topographic heterogeneity, this study reports the first thorough comparison of autoregulation in all major cerebral vessels.Methods: In forty healthy adults, flow velocity was monitored in the anterior, middle, and posterior cerebral arteries, and synchronized with arterial blood pressure. A transfer function analysis provided characteristics of autoregulation by quantifying the relationship between blood pressure and cerebral blood flow velocity.Results: Phase, which quantifies the time course of autoregulation, was similar in all vessels. Gain, which quantifies the magnitude of hemodynamic regulation, was lower in posterior cerebral artery, indicative of tighter regulation. However, after adjusting for baseline flow differences in each vascular territory, normalized gain was similar in all vessels.Conclusions: Discriminating dynamic cerebral autoregulation between cerebrovascular territories is feasible with a transcranial doppler based approach. In the posterior cerebral artery of healthy volunteers, absolute flow is more tightly regulated, but relative flow regulation is consistent across cerebrovascular territories.Significance: The methodology can be applied to focal disease states such as stroke or posterior reversible encephalopathy syndrome, in which the topographic distribution of autoregulation may be particularly critical.

scholarly journals Effects of heat stress on dynamic cerebral autoregulation during large fluctuations in arterial blood pressure

2009 ◽  
Vol 107 (6) ◽  
pp. 1722-1729 ◽  
Author(s):  
R. Matthew Brothers ◽  
Rong Zhang ◽  
Jonathan E. Wingo ◽  
Kimberly A. Hubing ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heat Stress ◽  
Arterial Blood Pressure ◽  
Cerebral Autoregulation ◽  
Lower Body Negative Pressure ◽  
Low Frequency ◽  
Thermal Conditions ◽  
Very Low Frequency ◽  
Arterial Blood ◽  
Dynamic Cerebral Autoregulation

Impaired cerebral autoregulation during marked reductions in arterial blood pressure may contribute to heat stress-induced orthostatic intolerance. This study tested the hypothesis that passive heat stress attenuates dynamic cerebral autoregulation during pronounced swings in arterial blood pressure. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity were continuously recorded for ∼6 min during normothermia and heat stress (core body temperature = 36.9 ± 0.1°C and 38.0 ± 0.1°C, respectively, P < 0.001) in nine healthy individuals. Swings in MAP were induced by 70-mmHg oscillatory lower body negative pressure (OLBNP) during normothermia and at a sufficient lower body negative pressure to cause similar swings in MAP during heat stress. OLBNP was applied at a very low frequency (∼0.03 Hz, i.e., 15 s on-15 s off) and a low frequency (∼0.1 Hz, i.e., 5 s on-5 s off). For each thermal condition, transfer gain, phase, and coherence function were calculated at both frequencies of OLBNP. During very low-frequency OLBNP, transfer function gain was reduced by heat stress (0.55 ± 0.20 and 0.31 ± 0.07 cm·s−1·mmHg−1 during normothermia and heat stress, respectively, P = 0.02), which is reflective of improved cerebrovascular autoregulation. During low-frequency OLBNP, transfer function gain was similar between thermal conditions (1.19 ± 0.53 and 1.01 ± 0.20 cm·s−1·mmHg−1 during normothermia and heat stress, respectively, P = 0.32). Estimates of phase and coherence were similar between thermal conditions at both frequencies of OLBNP. Contrary to our hypothesis, dynamic cerebral autoregulation during large swings in arterial blood pressure during very low-frequency (i.e., 0.03 Hz) OLBNP is improved during heat stress, but it is unchanged during low-frequency (i.e., 0.1 Hz) OLBNP.

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