scholarly journals Smoking Normalizes Cerebral Blood Flow and Oxygen Consumption after 12-Hour Abstention

2015 ◽  
Vol 35 (4) ◽  
pp. 699-705 ◽  
Author(s):  
Manouchehr S Vafaee ◽  
Albert Gjedde ◽  
Nasrin Imamirad ◽  
Kim Vang ◽  
Mallar M Chakravarty ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Analysis ◽  
Acute Effects ◽  
Cognitive Changes ◽  
Quantitative Pet ◽  
Nicotine Administration ◽  
Positron Emission ◽  
Historical Group ◽  
Cortical Regions

Acute nicotine administration stimulates [14C]deoxyglucose trapping in thalamus and other regions of rat brain, but acute effects of nicotine and smoking on energy metabolism have rarely been investigated in human brain by positron emission tomography (PET). We obtained quantitative PET measurements of cerebral blood flow (CBF) and metabolic rate of oxygen (CMRO2) in 12 smokers who had refrained from smoking overnight, and in a historical group of nonsmokers, testing the prediction that overnight abstinence results in widespread, coupled reductions of CBF and CMRO2. At the end of the abstention period, global grey-matter CBF and CMRO2 were both reduced by 17% relative to nonsmokers. At 15 minutes after renewed smoking, global CBF had increased insignificantly, while global CMRO2 had increased by 11%. Regional analysis showed that CMRO2 had increased in the left putamen and thalamus, and in right posterior cortical regions at this time. At 60 and 105 minutes after smoking resumption, CBF had increased by 8% and CMRO2 had increased by 11–12%. Thus, we find substantial and global impairment of CBF/CMRO2 in abstaining smokers, and acute restoration by resumption of smoking. The reduced CBF and CMRO2 during acute abstention may mediate the cognitive changes described in chronic smokers.

scholarly journals Regional and depth-dependence of cortical blood-flow assessed with high-resolution Arterial Spin Labeling (ASL)

2021 ◽  
pp. 0271678X2098238
Author(s):  
Manuel Taso ◽  
Fanny Munsch ◽  
Li Zhao ◽  
David C Alsop
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
High Resolution ◽  
Arterial Spin Labeling ◽  
Regional Analysis ◽  
Relaxation Times ◽  
Spin Labeling ◽  
High Resolution Mri ◽  
Cortical Cerebral Blood Flow ◽  
Cortical Regions

Methods for imaging of cerebral blood flow do not typically resolve the cortex and thus underestimate flow. However, recent work with high-resolution MRI has emphasized the regional and depth-dependent structural, functional and relaxation times variations within the cortex. Using high-resolution Arterial Spin Labeling (ASL) and T1 mapping acquisitions, we sought to probe the effects of spatial resolution and tissue heterogeneity on cortical cerebral blood flow (CBF) measurements with ASL. We acquired high-resolution (1.6mm) 3 whole brain ASL data in a cohort of 10 volunteers at 3T, along with T1 and transit-time (ATT) mapping, followed by group cortical surface-based analysis using FreeSurfer of the different measured parameters. Fully resolved regional analysis showed higher than average mid-thickness CBF in primary motor areas (+15%,p<0.002), frontal regions (+17%,p<0.01) and auditory cortex, while occipital regions had lower average CBF (-20%,p<10−5). ASL signal was higher towards the pial surface but correction for the shorter T1 near the white matter surface reverses this gradient, at least when using the low-resolution ATT map. Similar to structural measures, fully-resolved ASL CBF measures show significant differences across cortical regions. Depth-dependent variation of T1 in the cortex complicates interpretation of depth-dependent ASL signal and may have implications for the accurate CBF quantification at lower resolutions.

scholarly journals Decreases in Regional Cerebral Blood Flow with Normal Aging

1991 ◽  
Vol 11 (4) ◽  
pp. 684-689 ◽  
Author(s):  
Andrew J. Martin ◽  
Karl J. Friston ◽  
James G. Colebatch ◽  
Richard S. J. Frackowiak
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Regional Cerebral Blood Flow ◽  
Normal Aging ◽  
Regional Cerebral Blood ◽  
Cognitive Changes ◽  
Age Related ◽  
Positron Emission ◽  
Posterior Parietal ◽  
Parietal Cortices

Positron emission tomographic (PET) images of regional cerebral blood flow (rCBF) from 30 normal, resting volunteers aged 30 to 85 years were analysed to identify areas where rCBF fell with age. Images were anatomically normalised, and a pixel-by-pixel linear regression was performed to remove differences in global CBF between subjects. Pixels at which rCBF then showed a significant ( p < 0.01) negative correlation with age were identified. They were displayed as a statistical parametric map (SPM) of correlations. We demonstrate an age-related decrease in adjusted rCBF in the cingulate, parahippocampal, superior temporal, medial frontal, and posterior parietal cortices bilaterally, and in the left insular and left posterior prefrontal cortices (omnibus significance, χ2 = 2,291, p < 0.0001, df = 1). Decreases in rCBF suggest a regionally specific loss of cerebral function with age. The affected areas were all limbic, or association, cortices. Therefore, these decreases may constitute the cerebral substrate of the cognitive changes that occur during normal aging.

Changes in cerebral blood flow and carbohydrate metabolism during acute hyperketonemia

1996 ◽  
Vol 270 (5) ◽  
pp. E746-E751 ◽  
Author(s):  
S. G. Hasselbalch ◽  
P. L. Madsen ◽  
L. P. Hageman ◽  
K. S. Olsen ◽  
N. Justesen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Glucose Metabolism ◽  
Carbohydrate Metabolism ◽  
Ketone Bodies ◽  
Regional Analysis ◽  
Oxygen Metabolism ◽  
Blood Concentrations ◽  
Positron Emission ◽  
The Brain

During starvation, brain energy metabolism in humans changes toward oxidation of ketone bodies. To investigate if this shift is directly coupled to circulating blood concentrations of ketone bodies, we measured global cerebral blood flow (CBF) and global cerebral carbohydrate metabolism with the Kety-Schmidt technique before and during intravenous infusion with ketone bodies. During acute hyperketonemia (mean beta-hydroxybutyrate blood concentration 2.16 mM), cerebral uptake of ketones increased from 1.11 to 5.60 mumol.100 g-1.min-1, counterbalanced by an equivalent reduction of the cerebral glucose metabolism from 25.8 to 17.2 mumol.100 g-1.min-1, with the net result being an unchanged cerebral uptake of carbohydrates. In accordance with this, global cerebral oxygen metabolism was not significantly altered (144 vs. 135 mumol.100 g-1.min-1). The unchanged global cerebral metabolic activity was accompanied by a 39% increase in CBF from 51.0 to 70.9 ml.100 g-1.min-1. Regional analysis of the glucose metabolism by positron emission tomography-[18F]fluoro-2-deoxy-D-glucose indicated that mesencephalon does not oxidize ketone bodies to the same extent as the rest of the brain. It was concluded that the immediate oxidation of ketone bodies induced a decrease in cerebral glucose uptake in spite of an adequate glucose supply to the brain. Furthermore, acute hyperketonemia caused a resetting of the coupling between CBF and metabolism that could not be explained by alterations in arterial CO2 tension or pH.

scholarly journals Normal Pressure Hydrocephalus and Cerebral Blood Flow: A PET Study of Baseline Values

2004 ◽  
Vol 24 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Brian K. Owler ◽  
Shahan Momjian ◽  
Zofia Czosnyka ◽  
Marek Czosnyka ◽  
Alonso Péna ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Basal Ganglia ◽  
Normal Pressure Hydrocephalus ◽  
Regional Analysis ◽  
Region Of Interest ◽  
Normal Pressure ◽  
Positron Emission ◽  
Baseline Values

Regional cerebral blood flow (CBF) was studied with O15-water positron emission tomography and anatomic region-of-interest analysis on coregistered magnetic resonance in patients with idiopathic (n = 12) and secondary (n = 5) normal pressure hydrocephalus (NPH). Mean CBF was compared with values obtained from healthy volunteers (n = 12) and with clinical parameters. Mean CBF was significantly decreased in the cerebrum and cerebellum of patients with NPH. The regional analysis demonstrated that CBF was reduced in the basal ganglia and the thalamus but not in white matter regions. The results suggest that the role of the basal ganglia and thalamus in NPH may be more prominent than currently appreciated. The implications for theories regarding the pathogenesis of NPH are discussed.

Reversal of Focal Misery Perfusion after Intracranial Angioplasty: Case Report

Neurosurgery ◽  
2001 ◽  
Vol 48 (2) ◽  
pp. 436-440 ◽  
Author(s):  
Colin P. Derdeyn ◽  
DeWitte T. Cross ◽  
Christopher J. Moran ◽  
Ralph G. Dacey
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Artery ◽  
Intracranial Stenosis ◽  
Oxygen Extraction Fraction ◽  
Oxygen Extraction ◽  
Positron Emission ◽  
Misery Perfusion ◽  
Before And After ◽  
Hemodynamic Measurements

Abstract OBJECTIVE AND IMPORTANCE The presence of reduced blood flow and increased oxygen extraction fraction (OEF) (misery perfusion) in the hemisphere distal to an occluded carotid artery is a proven risk factor for subsequent stroke. Whether angioplasty of intracranial stenosis is sufficient to reverse this condition has not been documented. CLINICAL PRESENTATION A 67-year-old man exhibited progressive right hemispheric ischemic symptoms despite maximal antiplatelet and antithrombotic therapy. Angiography demonstrated focal 80% stenosis of the supraclinoid segment of the ipsilateral internal carotid artery. TECHNIQUE 15O positron emission tomographic measurements of cerebral blood flow and OEF were made before and after transfemoral percutaneous angioplasty. OEF values measured before angioplasty were elevated in the middle cerebral artery distal to the stenosis. Angioplasty reduced the degree of luminal stenosis to 40% (linear diameter). OEF values measured 36 hours after angioplasty were normal. CONCLUSION Angioplasty of intracranial stenosis can restore normal cerebral blood flow and oxygen extraction, despite mild residual stenosis after the procedure. Hemodynamic measurements may be useful for the identification of patients with the greatest potential to benefit from angioplasty.

scholarly journals Autoregulation of Cerebral Blood Flow to Changes in Arterial Pressure in Mild Alzheimer's Disease

2010 ◽  
Vol 30 (11) ◽  
pp. 1883-1889 ◽  
Author(s):  
Allyson R Zazulia ◽  
Tom O Videen ◽  
John C Morris ◽  
William J Powers
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Pressure ◽  
The Elderly ◽  
Local Defect ◽  
Clinical Dementia Rating ◽  
Positron Emission ◽  
Before And After

Studies in transgenic mice overexpressing amyloid precursor protein (APP) demonstrate impaired autoregulation of cerebral blood flow (CBF) to changes in arterial pressure and suggest that cerebrovascular dysfunction may be critically important in the development of pathological Alzheimer's disease (AD). Given the relevance of such a finding for guiding hypertension treatment in the elderly, we assessed autoregulation in individuals with AD. Twenty persons aged 75±6 years with very mild or mild symptomatic AD (Clinical Dementia Rating 0.5 or 1.0) underwent 15O-positron emission tomography (PET) CBF measurements before and after mean arterial pressure (MAP) was lowered from 107±13 to 92±9 mm Hg with intravenous nicardipine; 11C-PIB-PET imaging and magnetic resonance imaging (MRI) were also obtained. There were no significant differences in mean CBF before and after MAP reduction in the bilateral hemispheres (−0.9±5.2 mL per 100 g per minute, P=0.4, 95% confidence interval (CI)=−3.4 to 1.5), cortical borderzones (−1.9±5.0 mL per 100 g per minute, P=0.10, 95% CI=−4.3 to 0.4), regions of T2W-MRI-defined leukoaraiosis (−0.3±4.4 mL per 100 g per minute, P=0.85, 95% CI=−3.3 to 3.9), or regions of peak 11C-PIB uptake (−2.5±7.7 mL per 100 g per minute, P=0.30, 95% CI=−7.7 to 2.7). The absence of significant change in CBF with a 10 to 15 mm Hg reduction in MAP within the normal autoregulatory range demonstrates that there is neither a generalized nor local defect of autoregulation in AD.

scholarly journals Effects of Acetazolamide on Cerebral Blood Flow, Blood Volume, and Oxygen Metabolism: A Positron Emission Tomography Study with Healthy Volunteers

2001 ◽  
Vol 21 (12) ◽  
pp. 1472-1479 ◽  
Author(s):  
Hidehiko Okazawa ◽  
Hiroshi Yamauchi ◽  
Kanji Sugimoto ◽  
Hiroshi Toyoda ◽  
Yoshihiko Kishibe ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Capillary Blood ◽  
Emission Tomography ◽  
Positron Emission ◽  
Capillary Blood Volume

To evaluate changes in cerebral hemodynamics and metabolism induced by acetazolamide in healthy subjects, positron emission tomography studies for measurement of cerebral perfusion and oxygen consumption were performed. Sixteen healthy volunteers underwent positron emission tomography studies with15O-gas and water before and after intravenous administration of acetazolamide. Dynamic positron emission tomography data were acquired after bolus injection of H215O and bolus inhalation of15O2. Cerebral blood flow, metabolic rate of oxygen, and arterial-to-capillary blood volume images were calculated using the three-weighted integral method. The images of cerebral blood volume were calculated using the bolus inhalation technique of C15O. The scans for cerebral blood flow and volume and metabolic rate of oxygen after acetazolamide challenge were performed at 10, 20, and 30 minutes after drug injection. The parametric images obtained under the two conditions at baseline and after acetazolamide administration were compared. The global and regional values for cerebral blood flow and volume and arterial-to-capillary blood volume increased significantly after acetazolamide administration compared with the baseline condition, whereas no difference in metabolic rate of oxygen was observed. Acetazolamide-induced increases in both blood flow and volume in the normal brain occurred as a vasodilatory reaction of functioning vessels. The increase in arterial-to-capillary blood volume made the major contribution to the cerebral blood volume increase, indicating that the raise in cerebral blood flow during the acetazolamide challenge is closely related to arterial-to-capillary vasomotor responsiveness.

The acute effects of a polyphenol-rich blueberry beverage on cerebral blood flow

Appetite ◽  
2016 ◽  
Vol 101 ◽  
pp. 227
Author(s):  
G.F. Dodd ◽  
C. Moutsiana ◽  
J.P.E. Spencer ◽  
L.T. Butler
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Acute Effects

Neural Mechanism of Propofol Anesthesia in Severe Depression

2003 ◽  
Vol 98 (5) ◽  
pp. 1101-1111 ◽  
Author(s):  
Kenichi Ogawa ◽  
Takeshi Uema ◽  
Nobutaka Motohashi ◽  
Masami Nishikawa ◽  
Harumasa Takano ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Statistical Parametric Mapping ◽  
Severe Depression ◽  
Dose Effect ◽  
Emission Tomography ◽  
Association Cortex ◽  
Depressed Patients ◽  
Positron Emission

Background The precise neural mechanisms of propofol anesthesia in humans are still unknown. The authors examined the acute effects of propofol on regional cerebral blood flow (rCBF) using positron emission tomography in patients with severe depression. Methods In six severely depressed patients (mean age, 55.0 yr) scheduled for electroconvulsive therapy, anesthetic levels were monitored by electroencephalography, and rCBF was serially quantified in the awake, sedated, and anesthetized states. The authors used high-resolution positron emission tomography with 15O-labeled water and statistical parametric mapping 99 for imaging and analysis of the data. Results Global cerebral blood flow showed sharp decreases from the awake level during the administration of propofol, decreasing 26.8% in the sedated state and 54.4% in the anesthetized state. Moreover, a dose effect was seen in both parietal cortices and the left lateral prefrontal region with larger regions of relative decrease in rCBF at higher propofol doses. At the higher dose, the values of rCBF in the pulvinar nucleus of the thalamus, the pontine tegmentum, and the cerebellar cortex were also affected. Meanwhile, there were few changes of relative rCBF in the basal frontal lobes during both sedated and anesthetized states. Conclusions As in earlier studies using normal subjects, pronounced suppression in rCBF in the brain stem reticular formation, the thalamus, and the parietal association cortex occurred even in severely depressed patients. However, previously reported decreases in rCBF in the basal frontal lobe were absent in depressed patients.

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