scholarly journals A theoretical framework for estimating cerebral oxygen metabolism changes using the calibrated-BOLD method: Modeling the effects of blood volume distribution, hematocrit, oxygen extraction fraction, and tissue signal properties on the BOLD signal

NeuroImage ◽  
2011 ◽  
Vol 58 (1) ◽  
pp. 198-212 ◽  
Author(s):  
Valerie E.M. Griffeth ◽  
Richard B. Buxton
Keyword(s):  
Blood Volume ◽  
Oxygen Metabolism ◽  
Theoretical Framework ◽  
Oxygen Extraction Fraction ◽  
Volume Distribution ◽  
Cerebral Oxygen ◽  
Bold Signal ◽  
Cerebral Oxygen Metabolism ◽  
Extraction Fraction ◽  
Blood Volume Distribution

scholarly journals Hemodynamic and metabolic changes during hypercapnia with normoxia and hyperoxia using pCASL and TRUST MRI in healthy adults

2021 ◽  
pp. 0271678X2110645
Author(s):  
Pieter T Deckers ◽  
Alex A Bhogal ◽  
Mathijs BJ Dijsselhof ◽  
Carlos C Faraco ◽  
Peiying Liu ◽  
...  
Keyword(s):  
Arterial Spin Labeling ◽  
Oxygen Metabolism ◽  
Blood Oxygenation Level Dependent ◽  
Blood Oxygenation ◽  
Cerebrovascular Reactivity ◽  
Oxygen Extraction Fraction ◽  
Mixed Effect ◽  
Cerebral Oxygen Metabolism ◽  
Extraction Fraction ◽  
Oxygenation Level

Blood oxygenation level-dependent (BOLD) or arterial spin labeling (ASL) MRI with hypercapnic stimuli allow for measuring cerebrovascular reactivity (CVR). Hypercapnic stimuli are also employed in calibrated BOLD functional MRI for quantifying neuronally-evoked changes in cerebral oxygen metabolism (CMRO2). It is often assumed that hypercapnic stimuli (with or without hyperoxia) are iso-metabolic; increasing arterial CO2 or O2 does not affect CMRO2. We evaluated the null hypothesis that two common hypercapnic stimuli, ‘CO2 in air’ and carbogen, are iso-metabolic. TRUST and ASL MRI were used to measure the cerebral venous oxygenation and cerebral blood flow (CBF), from which the oxygen extraction fraction (OEF) and CMRO2 were calculated for room-air, ‘CO2 in air’ and carbogen. As expected, CBF significantly increased (9.9% ± 9.3% and 12.1% ± 8.8% for ‘CO2 in air’ and carbogen, respectively). CMRO2 decreased for ‘CO2 in air’ (−13.4% ± 13.0%, p < 0.01) compared to room-air, while the CMRO2 during carbogen did not significantly change. Our findings indicate that ‘CO2 in air’ is not iso-metabolic, while carbogen appears to elicit a mixed effect; the CMRO2 reduction during hypercapnia is mitigated when including hyperoxia. These findings can be important for interpreting measurements using hypercapnic or hypercapnic-hyperoxic (carbogen) stimuli.

scholarly journals PET Quantification of Cerebral Oxygen Metabolism in Small Animals

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Takashi Temma ◽  
Kazuhiro Koshino ◽  
Tetsuaki Moriguchi ◽  
Jun-ichiro Enmi ◽  
Hidehiro Iida
Keyword(s):  
Cerebral Blood Volume ◽  
Animal Experiments ◽  
Oxygen Metabolism ◽  
Cerebrovascular Diseases ◽  
Oxygen Extraction Fraction ◽  
Small Animals ◽  
Cerebral Oxygen ◽  
Technical Problems ◽  
Cerebral Oxygen Metabolism

Understanding cerebral oxygen metabolism is of great importance in both clinical diagnosis and animal experiments because oxygen is a fundamental source of brain energy and supports brain functional activities. Since small animals such as rats are widely used to study various diseases including cerebral ischemia, cerebrovascular diseases, and neurodegenerative diseases, the development of a noninvasivein vivomeasurement method of cerebral oxygen metabolic parameters such as oxygen extraction fraction (OEF) and cerebral metabolic rate of oxygen (CMRO2) as well as cerebral blood flow (CBF) and cerebral blood volume (CBV) has been a priority. Although positron emission tomography (PET) with15O labeled gas tracers has been recognized as a powerful way to evaluate cerebral oxygen metabolism in humans, this method could not be applied to rats due to technical problems and there were no reports of PET measurement of cerebral oxygen metabolism in rats until an15O-O2injection method was developed a decade ago. Herein, we introduce an intravenous administration method using two types of injectable15O-O2and an15O-O2gas inhalation method through an airway placed in the trachea, which enables oxygen metabolism measurements in rats.

scholarly journals Cerebral Oxygen Metabolism after Aneurysmal Subarachnoid Hemorrhage

1991 ◽  
Vol 11 (5) ◽  
pp. 837-844 ◽  
Author(s):  
David A. Carpenter ◽  
Robert L. Grubb ◽  
Lee W. Tempel ◽  
William J. Powers
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Oxygen Metabolism ◽  
Brain Regions ◽  
Aneurysm Rupture ◽  
Oxygen Extraction Fraction ◽  
Intracerebral Hematoma ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Primary Reduction

Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure the regional cerebral metabolic rate for oxygen (rCMRO2), oxygen extraction fraction (rOEF), and cerebral blood flow (rCBF) 16 times in 11 patients with aneurysmal SAH. All studies were performed preoperatively; no patient had hydrocephalus or intracerebral hematoma on brain CT. Eight patients with no arteriographic vasospasm who were studied on days 1–4 post-SAH had a significant 25% reduction in global CMRO2 compared to age-matched controls, and no significant change in global OEF, suggesting a primary reduction in CMRO2 caused by SAH. Four patients studied seven times during arteriographic vasospasm had significantly increased rOEF with unchanged CMRO2 in arterial territories affected by arteriographic vasospasm compared to territories without vasospasm, indicative of cerebral ischemia without infarction. No brain regions studied with PET were infarcted on follow-up CT. We conclude that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia.

scholarly journals Quantitative mapping of cerebral oxygen metabolism using breath-hold calibrated fMRI

2021 ◽  
Author(s):  
Michael Germuska ◽  
Rachael C Stickland ◽  
Antonio Maria Chiarelli ◽  
Hannah L Chandler ◽  
Richard G Wise
Keyword(s):  
Blood Flow ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Arterial Oxygen ◽  
Breath Holding ◽  
Breath Hold ◽  
Neural Function ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism

Magnetic resonance imaging (MRI) offers the possibility to non-invasively map the rate of cerebral metabolic oxygen consumption (CMRO2), which is essential for understanding and monitoring neural function in both health and disease. Existing methods of mapping CMRO2, based on respiratory modulation of arterial spin labelling (ASL) and blood oxygen level dependent (BOLD) signals, require lengthy acquisitions and independent modulation of both arterial oxygen and carbon dioxide levels. Here, we present a new simplified method for mapping the rate of cerebral oxygen metabolism that can be performed using a simple breath-holding paradigm. The method incorporates flow-diffusion modelling of oxygen transport and physiological constraints to create a non-linear mapping between the maximum BOLD signal, M, baseline blood flow (CBF0), and CMRO2. A gradient boosted decision tree is used to learn this mapping directly from simulated MRI data. Modelling studies demonstrate that the proposed method is robust to variation in cerebral physiology and metabolism. This new gas-free methodology offers a rapid and pragmatic alternative to existing dual-calibrated methods, removing the need for specialist respiratory equipment and long acquisition times. In-vivo testing of the method, using an 8-minute 45 second protocol of repeated breath-holding, was performed on 15 healthy volunteers, producing quantitative maps of cerebral blood flow (CBF), oxygen extraction fraction (OEF), and CMRO2.

scholarly journals Incidence and Mechanisms of Cerebral Ischemia in Early Clinical Head Injury

2004 ◽  
Vol 24 (2) ◽  
pp. 202-211 ◽  
Author(s):  
Jonathan P. Coles ◽  
Tim D. Fryer ◽  
Piotr Smielewski ◽  
Doris A. Chatfield ◽  
Luzius A. Steiner ◽  
...  
Keyword(s):  
Head Injury ◽  
Oxygen Metabolism ◽  
Jugular Bulb ◽  
Emission Tomography ◽  
Oxygen Extraction Fraction ◽  
Ischemic Brain ◽  
Cerebral Oxygen Metabolism ◽  
Extraction Fraction ◽  
Positron Emission ◽  
The Brain

Antemortem demonstration of ischemia has proved elusive in head injury because regional CBF reductions may represent hypoperfusion appropriately coupled to hypometabolism. Fifteen patients underwent positron emission tomography within 24 hours of head injury to map cerebral blood flow (CBF), cerebral oxygen metabolism (CMRO2), and oxygen extraction fraction (OEF). We estimated the volume of ischemic brain (IBV) and used the standard deviation of the OEF distribution to estimate the efficiency of coupling between CBF and CMRO2. The IBV in patients was significantly higher than controls (67 ± 69 vs. 2 ± 3 mL; P < 0.01). The coexistence of relative ischemia and hyperemia in some patients implies mismatching of perfusion to oxygen use. Whereas the saturation of jugular bulb blood (SjO2) correlated with the IBV ( r = 0.8, P < 0.01), SjO2 values of 50% were only achieved at an IBV of 170 ± 63 mL (mean ± 95% CI), which equates to 13 ± 5% of the brain. Increases in IBV correlated with a poor Glasgow Outcome Score 6 months after injury (ρ = −0.6, P < 0.05). These results suggest significant ischemia within the first day after head injury. The ischemic burden represented by this “traumatic penumbra” is poorly detected by bedside clinical monitors and has significant associations with outcome.

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