Response of Cerebral Blood Flow and Blood Pressure to Dynamic Exercise: A Study Using PET

2018 ◽  
Vol 39 (03) ◽  
pp. 181-188 ◽  
Author(s):  
Mikio Hiura ◽  
Tadashi Nariai ◽  
Muneyuki Sakata ◽  
Akitaka Muta ◽  
Kenji Ishibashi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Stem ◽  
Cardiovascular Response ◽  
Human Subjects ◽  
Insular Cortex ◽  
Brain Regions ◽  
Dynamic Exercise ◽  
The Brain

AbstractDynamic exercise elicits fluctuations in blood pressure (BP) and cerebral blood flow (CBF). This study investigated responses in BP and CBF during cycling exercise and post-exercise hypotension (PEH) using positron emission tomography (PET). CBF was measured using oxygen-15-labeled water (H2 15O) and PET in 11 human subjects at rest (Rest), at the onset of exercise (Ex1), later in the exercise (Ex2), and during PEH. Global CBF significantly increased by 13% at Ex1 compared with Rest, but was unchanged at Ex2 and during PEH. Compared with at Rest, regional CBF (rCBF) increased at Ex1 (20~42%) in the cerebellar vermis, sensorimotor cortex for the bilateral legs (M1Leg and S1Leg), insular cortex and brain stem, but increased at Ex2 (28~31%) only in the vermis and M1Leg and S1Leg. During PEH, rCBF decreased compared with Rest (8~13%) in the cerebellum, temporal gyrus, piriform lobe, thalamus and pons. The areas showing correlations between rCBF and mean BP during exercise and PEH were consistent with the central autonomic network, including the brain stem, cerebellum, and hypothalamus (R2=0.25–0.64). The present study suggests that higher brain regions are coordinated through reflex centers in the brain stem in order to regulate the cardiovascular response to exercise.

Cerebral Blood Flow during Dynamic Exercise Correlates with Blood Pressure in Autonomic Brain Regions

2017 ◽  
Vol 49 (5S) ◽  
pp. 824
Author(s):  
Mikio Hiura ◽  
Akitaka Muta ◽  
Muneyuki Sakata ◽  
Satoshi Wagatsuma ◽  
Tetsurou Tago ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Regions ◽  
Dynamic Exercise

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

Cerebral blood flow and energy metabolism during stress

1990 ◽  
Vol 259 (2) ◽  
pp. H269-H280 ◽  
Author(s):  
R. M. Bryan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Energy Metabolism ◽  
Adrenergic Receptor ◽  
Conditioned Fear ◽  
Brain Regions ◽  
Stressful Events ◽  
Ethanol Withdrawal ◽  
Adrenergic Mechanism ◽  
The Brain

Many, but not all, stressful events are accompanied by increases in cerebral blood flow and/or energy metabolism. The stressful events include pharmacological paralysis, footshock, conditioned fear, hypotension, hypoglycemia, hypoxia, noise, and ethanol withdrawal. These increases are significant because 1) all brain regions are often affected, i.e., certain stressful events have global effects on cerebral blood flow and energy metabolism; and 2) various stressful events appear to have a common adrenergic mechanism for increasing cerebral blood flow and energy metabolism. The adrenergic mechanism involves beta-adrenergic receptor stimulation by either epinephrine secreted from the adrenal medulla or possibly norepinephrine endogenous to the brain. While adrenergic mechanisms are not the only mechanism controlling flow and metabolism for a given stressful condition, they do appear to be common to many situations. At least part of the increase in cerebral blood flow and energy metabolism during many conditions appears to be the result of the stress response and not directly a result of the condition itself.

Effect of hypoxia and hypercapnia on neurohypophyseal blood flow

1986 ◽  
Vol 250 (1) ◽  
pp. H7-H15
Author(s):  
D. F. Hanley ◽  
D. A. Wilson ◽  
R. J. Traystman
Keyword(s):  
Blood Pressure ◽  
Carbon Monoxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Brain Regions ◽  
Regulatory Mechanisms ◽  
Similar Increase ◽  
Regional Cerebral Blood ◽  
Pressure Controlled

Neurohypophyseal blood flow responses to hypoxia and hypercapnia were studied in pentobarbital anesthetized, paralyzed dogs. Arterial O2 content was lowered from control (18 +/- 2 vol%) to 8 +/- 1 vol% by either decreasing O2 tension (hypoxic hypoxia, HH) or by increasing carboxyhemoglobin saturation (carbon monoxide hypoxia, COH) at normal O2 tension. In all animals HH and COH resulted in similar increases in total cerebral blood flow (239 and 300%, respectively). Regional cerebral blood flow showed a similar increase for all brain regions except the neurohypophysis (NH). The NH increased its blood flow with HH (approximately 320% of control) but was unchanged with COH (117% of control). The responsiveness of NH blood vessels was tested under conditions of hypercapnia (10% CO2) and HH with blood pressure controlled by concurrent hemorrhage. The response of NH vessels to altered arterial O2 tension occurs independently of blood pressure. Systemic [H+] or CO2 tension produce only small changes in NH blood flow. These data suggest that hypoxic and hypercapnic regulatory mechanisms for the NH are different from those of other brain regions. The precise mechanism by which the NH hypoxic response occurs remains unclear, but our data suggest an important role for systemic arterial O2 tension and chemoreceptors.

Relationship between Cardiopulmonary Bypass Flow Rate and Cerebral Embolization in Dogs 

1999 ◽  
Vol 91 (5) ◽  
pp. 1387-1387 ◽  
Author(s):  
Hulya Sungurtekin ◽  
Walter Plöchl ◽  
David J. Cook
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cardiopulmonary Bypass ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Rank Order ◽  
Brain Regions ◽  
Pump Flow ◽  
Cerebral Embolization ◽  
The Brain

Background Cerebral embolization is a primary cause of cardiac surgical neurologic morbidity. During cardiopulmonary bypass (CPB), there are well-defined periods of embolic risk. In theory, cerebral embolization might be reduced by an increase in pump flow during these periods. The purpose of this study was to determine the CPB flow-embolization relation in a canine model. Methods Twenty mongrel dogs underwent CPB at 35 degrees C with alpha-stat management and a fentanyl-midazolam anesthetic. In each animal, CPB flow was adjusted to achieve a mean arterial pressure of 65-75 mmHg. During CPB, an embolic load of 1.2 x 10(5) 67 microm fluorescent microspheres was injected into the arterial inflow line. Before and after embolization, cerebral blood flow was determined using 15-microm microspheres. Tissue was taken from 12 brain regions and microspheres were recovered. The relation between pump flow and embolization/g of brain was determined. Results The mean arterial pressure at embolization was 67 +/-4 mmHg, and the range of pump flow was 0.9-3.5 l x min(-1)x m(-2). Cerebral blood flow was independent of pump flow. At lower pump flow, the percentage of that flow delivered to the brain increased. There was a strong inverse relation between pump flow and cerebral embolization (r = -0.708, P < 0.000 by Spearman rank order correlation). Conclusions Cerebral embolization is determined by the CPB flow. At an unchanged mean arterial pressure, as pump flow is reduced, a progressively greater proportion of that flow is delivered to the brain.

Relationship between cardiac output and cerebral blood flow in patients with intact and with impaired autoregulation

1990 ◽  
Vol 73 (3) ◽  
pp. 368-374 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Blood Viscosity ◽  
Volume Expansion ◽  
Physiological Mechanism ◽  
Brain Regions ◽  
Intravascular Volume ◽  
Wide Range

✓ Intravascular volume expansion has been successfully employed to promote blood flow in ischemic brain regions. This effect has been attributed to both decreased blood viscosity and increased cardiac output resulting from volume expansion. The physiological mechanism by which changes in cardiac output would affect cerebral blood flow (CBF), independent of blood pressure variations, is unclear, but impaired cerebral autoregulation is believed to play a role. In order to evaluate the relationship between cardiac output and CBF when autoregulation is either intact or defective, 135 simultaneous measurements of cardiac output (thermodilution method) and CBF (by the 133Xe inhalation or intravenous injection method) were performed in 35 severely head-injured patients. In 81 instances, these measurements were performed after manipulation of blood pressure with phenylephrine or Arfonad (trimethaphan camsylate), or manipulation of blood viscosity with mannitol. Autoregulation was found to be intact in 55 of these cases and defective in 26. A wide range of changes in cardiac output occurred after administration of each drug. No correlation existed between the changes in cardiac output and the changes in CBF, regardless of the status of blood pressure autoregulation. A significant (40%) increase in CBF was found after administration of mannitol when autoregulation was defective. These data support the hypothesis that, within broad limits, CBF is not related to cardiac output, even when autoregulation is impaired. Thus, the effect of intravascular volume expansion appears to be mediated by decreased blood viscosity rather than cardiac output augmentation.

scholarly journals Effects of Immobilization Stress on Cerebral Blood Flow and Cerebrovascular Permeability in Spontaneously Hypertensive Rats

1982 ◽  
Vol 2 (3) ◽  
pp. 373-379 ◽  
Author(s):  
M. Ohata ◽  
H. Takei ◽  
W. R. Fredericks ◽  
S. I. Rapoport
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Brain Regions ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Brain Barrier Permeability ◽  
Cerebrovascular Permeability ◽  
Area Product ◽  
The Brain

Immobilization of unanesthetized, freely breathing, 10–12-month-old, spontaneously hypertensive rats (SHR) did not significantly alter regional cerebral blood flow (rCBF) in 13 of 14 brain regions assayed. After 5 or 15 min of immobilization, rCBF was unchanged except at the frontal lobe, where it rose significantly by 21%. Furthermore, immobilization did not increase the cerebrovascular permeability–area product for 14C-sucrose, except at three brain regions. The results indicate that immobilization of SHR does not significantly affect rCBF or blood–brain barrier permeability in most regions of the brain, and suggest that adequate autoregulation of rCBF is maintained under stress.

Cerebral Blood Flow in the Brain Stem During Increased ICP

1983 ◽  
pp. 452-457 ◽  
Author(s):  
J. Zierski ◽  
E. Kurzaj ◽  
O. Hoffmann ◽  
B. Winkler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Stem ◽  
The Brain ◽  
Increased Icp

scholarly journals The Retention of [99mTc]-d,l-HM-PAO in the Human Brain after Intracarotid Bolus Injection: A Kinetic Analysis

1988 ◽  
Vol 8 (1_suppl) ◽  
pp. S13-S22 ◽  
Author(s):  
Niels A. Lassen ◽  
Allan R. Andersen ◽  
Lars Friberg ◽  
Olaf B. Paulson
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Kinetic Model ◽  
Rate Constant ◽  
Human Subjects ◽  
Blood Pool ◽  
Partition Ratio ◽  
Clearance Ratio ◽  
Efflux Rate Constant ◽  
The Brain

[99mTc]– d,l-HM-PAO (HM-PAO) was injected rapidly into the internal carotid artery and its retention in the brain was recorded by external scintillation cameras in eight human subjects. A model is described based on three compartments: the lipophilic tracer in the blood pool of the brain, the lipophilic tracer inside the brain, and the hydrophilic form retained in the brain. The retention curve initially drops abruptly, corresponding to the nonextracted fraction of the injectate leaving the brain; it then falls exponentially towards the asymptotic level of the fractional steady-state retention R. Cerebral blood flow ( F) was measured using the xenon-133 intracarotid injection method. The first-pass extraction E of HM-PAO was calculated from F using an empiric regression equation. The residue curves for the whole brain after intracarotid HM-PAO injection were analyzed to yield a retention fraction ( R') and the brain clearance backflux constant of lipophilic HM-PAO ( k). From the kinetic model and the measured values of R', k, and F, the following parameter values could be calculated: the average retained fraction of all tracer supplied to the brain, R = 0.38 ± 0.05 (mean ± SD), the conversion rate constant (lipophilic to hydrophilic tracer) in the brain k3 = 0.80 ± 0.12 min− 1, the efflux rate constant (brain to blood) k2 = 0.69 ± 0.11 min− 1, the conversion/clearance ratio α = k3/ k2 = 1.18 ± 0.25, the influx (blood clearance) constant K1 = 0.45 ± 0.11 ml/g/min, and the brain/blood partition ratio Λ = K1/ k2 = 0.67 ± 0.23 ml/g. Using the kinetic model and assuming constancy of α, an algorithm was developed that corrects for the blood flow dependent backflux of HM-PAO and results in a more linear relation between regional cerebral blood flow (rCBF) and HM-PAO distribution.

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