scholarly journals Multiscale modeling and simulation of brain blood flow

2016 ◽  
Vol 28 (2) ◽  
pp. 021304 ◽  
Author(s):  
Paris Perdikaris ◽  
Leopold Grinberg ◽  
George Em Karniadakis
Keyword(s):  
Blood Flow ◽  
Modeling And Simulation ◽  
Multiscale Modeling ◽  
Brain Blood Flow

Heterogeneity of Cerebral Blood Flow: a Fractal Approach

2000 ◽  
Vol 39 (02) ◽  
pp. 37-42 ◽  
Author(s):  
P. Hartikainen ◽  
J. T. Kuikka
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Fractal Dimension ◽  
Frontal Lobe ◽  
Fractal Analysis ◽  
Relative Dispersion ◽  
Emission Computed Tomography ◽  
Brain Blood Flow ◽  
Healthy Controls ◽  
Fractal Approach

Summary Aim: We demonstrate the heterogeneity of regional cerebral blood flow using a fractal approach and singlephoton emission computed tomography (SPECT). Method: Tc-99m-labelled ethylcysteine dimer was injected intravenously in 10 healthy controls and in 10 patients with dementia of frontal lobe type. The head was imaged with a gamma camera and transaxial, sagittal and coronal slices were reconstructed. Two hundred fifty-six symmetrical regions of interest (ROIs) were drawn onto each hemisphere of functioning brain matter. Fractal analysis was used to examine the spatial heterogeneity of blood flow as a function of the number of ROIs. Results: Relative dispersion (= coefficient of variation of the regional flows) was fractal-like in healthy subjects and could be characterized by a fractal dimension of 1.17 ± 0.05 (mean ± SD) for the left hemisphere and 1.15 ± 0.04 for the right hemisphere, respectively. The fractal dimension of 1.0 reflects completely homogeneous blood flow and 1.5 indicates a random blood flow distribution. Patients with dementia of frontal lobe type had a significantly lower fractal dimension of 1.04 ± 0.03 than in healthy controls. Conclusion: Within the limits of spatial resolution of SPECT, the heterogeneity of brain blood flow is well characterized by a fractal dimension. Fractal analysis may help brain scientists to assess age-, sex- and laterality-related anatomic and physiological changes of brain blood flow and possibly to improve precision of diagnostic information available for patient care.

Effects of smoking marijuana on focal attention and brain blood flow

2007 ◽  
Vol 22 (3) ◽  
pp. 135-148 ◽  
Author(s):  
Daniel S. O'Leary ◽  
Robert I. Block ◽  
Julie A. Koeppel ◽  
Susan K. Schultz ◽  
Vincent A. Magnotta ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Blood Flow ◽  
Focal Attention ◽  
Smoking Marijuana

Modeling Cerebral Blood Flow and Ventilation Instability due to CO2

2021 ◽  
Author(s):  
Stanley M. Yamashiro ◽  
Takahide Kato
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Current Model ◽  
Respiratory Control ◽  
Breath Hold ◽  
Chronic Obstructive ◽  
Brain Blood Flow ◽  
Linear Interaction ◽  
Non Linear ◽  
Flow Changes

A minimal model of cerebral blood flow and respiratory control was developed to describe hypocapnic and hypercapnic responses. Important non-linear properties such as cerebral blood flow changes with arterial partial pressure of carbon dioxide (PaCO2) and associated time dependent circulatory time delays were included. It was also necessary to vary cerebral metabolic rate as a function of PaCO2. The cerebral blood flow model was added to a previously developed respiratory control model to simulate central and peripheral controller dynamics for humans. Model validation was based on previously collected data. The variable time delay due to brain blood flow changes in hypercapnia was an important determinant of predicted instability due to non-linear interaction in addition to linear loop gain considerations. Peripheral chemoreceptor gains above a critical level, but within normal limits, was necessary to produce instability. Instability was observed in recovery from hypercapnia and hypocapnia. The 20 sec breath-hold test appears to be a simple test of brain blood flow mediated instability in hypercapnia. Brain blood flow was predicted to play an important role with non-linear properties. There is an important interaction predicted by the current model between central and peripheral control mechanisms related to instability in hypercapnia recovery. Post hyperventilation breathing pattern can also reveal instability tied to brain blood flow. Previous data collected in patients with chronic obstructive lung disease was closely fitted with the current model and instability predicted. Brain vascular volume was proposed as a potential cause of instability despite cerebral autoregulation promoting constant brain flow.

Interactions of increased pO2 and pCO2 effects in producing convulsions and death in mice

1961 ◽  
Vol 16 (1) ◽  
pp. 1-7 ◽  
Author(s):  
John R. Marshall ◽  
Christian J. Lambertsen
Keyword(s):  
Carbon Dioxide ◽  
High Pressure ◽  
Blood Flow ◽  
Latent Period ◽  
Survival Time ◽  
Brain Blood Flow ◽  
Time Data ◽  
Cortical Depression ◽  
Survival Time Data ◽  
Very High

In 379 mice subjected to from 1 to 11 atm. of pO2 and 0 to 304 mm Hg of pCO2 for 90 minutes, oxygen was convulsigenic at pressures greater than 3 atm. and lethal at greater than 4 atm. Carbon dioxide in 1 atm. of O2 was not convulsigenic but was lethal at very high tensions. In the presence of O2 at high pressure (OHP) small elevations of CO2 tension shortened the preconvulsive latent period, whereas CO2 tensions greater than 120 mm Hg inhibited convulsions. Survival time in OHP was shortened by the addition of CO2. An interaction between OHP and CO2 effects is suggested by both the preconvulsive latent period and survival time data. The effects of CO2 on OHP and electroshock convulsions are compared and possible reasons for differences are discussed in light of the previously demonstrated general cortical depression and inhibition of convulsions by CO2. The potentiation of OHP convulsions by low CO2 tensions is probably due to effects on brain blood flow. Although death can occur without convulsions there is a tendency for animals susceptible to convulsions to be also susceptible to the lethal properties of OHP with CO2. Submitted on July 28, 1960

No effect of brain blood flow on ventilatory depression during sustained hypoxia

1989 ◽  
Vol 66 (4) ◽  
pp. 1674-1678 ◽  
Author(s):  
A. Suzuki ◽  
M. Nishimura ◽  
H. Yamamoto ◽  
K. Miyamoto ◽  
F. Kishi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Brain Tissue ◽  
Initial Phase ◽  
Intermediate Phase ◽  
Minute Ventilation ◽  
Brain Blood Flow ◽  
Final Phase ◽  
Venous Pco2 ◽  
Tissue Pco2 ◽  
Sustained Hypoxia

Minute ventilation (VE) during sustained hypoxia is not constant but begins to decline within 10–25 min in adult humans. The decrease in brain tissue PCO2 may be related to this decline in VE, because hypoxia causes an increase in brain blood flow, thus resulting in enhanced clearance of CO2 from the brain tissue. To examine the validity of this hypothesis, we measured VE and arterial and internal jugular venous blood gases simultaneously and repeatedly in 15 healthy male volunteers during progressive and subsequent sustained isocapnic hypoxia (arterial PO2 = 45 Torr) for 20 min. It was assumed that jugular venous PCO2 was an index of brain tissue PCO2. Mean VE declined significantly from the initial (16.5 l/min) to the final phase (14.1 l/min) of sustained hypoxia (P less than 0.05). Compared with the control (50.9 Torr), jugular venous PCO2 significantly decreased to 47.4 Torr at the initial phase of hypoxia but did not differ among the phases of hypoxia (47.2 Torr for the intermediate phase and 47.7 Torr for the final phase). We classified the subjects into two groups by hypoxic ventilatory response during progressive hypoxia at the mean value. The decrease in VE during sustained hypoxia was significant in the low responders (n = 9) [13.2 (initial phase) to 9.3 l/min (final phase of hypoxia), P less than 0.01], but not in the high responders (n = 6) (20.9–21.3 l/min, NS). This finding could not be explained by the change of arterial or jugular venous gases, which did not significantly change during sustained hypoxia in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

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