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 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 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 Concurrent tissue oxymetry and blood flowmetry to assess the effect of drugs on cerebral oxygen metabolism

2020 ◽  
Vol 10 (3) ◽  
pp. 5552-5555
Keyword(s):  
Brain Activity ◽  
Oxygen Metabolism ◽  
Brain Regions ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Cns Depressant ◽  
Carbon Dioxide Co2 ◽  
Blood Flowmetry ◽  
The Brain

An Oxylite/LDF system (Oxford Optronix, UK) driven by a sensor made of optical fibres for the tissue oxygen tension (pO2) and for the Laser Doppler Blood Flow (BF) was implemented. This has allowed pO2 and BF real time measurements in discrete brain areas of anaesthetised rats that were then challenged with exogenous oxygen (O2) and carbon dioxide (CO2). The results gathered were compared with data obtained following treatment with drugs that have excitatory influence upon the brain activity such as amphetamine or with a central nervous system (CNS) depressant such as CI-966. Altogether these experiments support the methodology for in vivo investigation of pharmacological effects on cerebral oxygen metabolism and could provide new understandings on the effects of psychostimulants and anticonvulsants on selected brain regions.

scholarly journals Cerebral Oxygen Metabolism in Neonatal Hypoxic Ischemic Encephalopathy during and after Therapeutic Hypothermia

2013 ◽  
Vol 34 (1) ◽  
pp. 87-94 ◽  
Author(s):  
Mathieu Dehaes ◽  
Alpna Aggarwal ◽  
Pei-Yi Lin ◽  
C Rosa Fortuno ◽  
Angela Fenoglio ◽  
...  
Keyword(s):  
Blood Flow ◽  
Therapeutic Hypothermia ◽  
Cerebral Blood Volume ◽  
Matched Control ◽  
Oxygen Metabolism ◽  
Correlation Spectroscopy ◽  
Hypoxic Ischemic Encephalopathy ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Ischemic Encephalopathy

Pathophysiologic mechanisms involved in neonatal hypoxic ischemic encephalopathy (HIE) are associated with complex changes of blood flow and metabolism. Therapeutic hypothermia (TH) is effective in reducing the extent of brain injury, but it remains uncertain how TH affects cerebral blood flow ( CBF) and metabolism. Ten neonates undergoing TH for HIE and seventeen healthy controls were recruited from the NICU and the well baby nursery, respectively. A combination of frequency domain near infrared spectroscopy (FDNIRS) and diffuse correlation spectroscopy (DCS) systems was used to non-invasively measure cerebral hemodynamic and metabolic variables at the bedside. Results showed that cerebral oxygen metabolism ( CMRO 2i) and CBF indices ( CBF i) in neonates with HIE during TH were significantly lower than post-TH and age-matched control values. Also, cerebral blood volume ( CBV) and hemoglobin oxygen saturation ( SO 2) were significantly higher in neonates with HIE during TH compared with age-matched control neonates. Post-TH CBV was significantly decreased compared with values during TH whereas SO 2 remained unchanged after the therapy. Thus, FDNIRS–DCS can provide information complimentary to SO 2 and can assess individual cerebral metabolic responses to TH. Combined FDNIRS–DCS parameters improve the understanding of the underlying physiology and have the potential to serve as bedside biomarkers of treatment response and optimization.

scholarly journals Preserved Cerebral Oxygen Metabolism in Astrocytic Dysfunction: A Combination Study of 15O-Gas PET with 14C-Acetate Autoradiography

2019 ◽  
Vol 9 (5) ◽  
pp. 101 ◽  
Author(s):  
Carla Mari Macaisa ◽  
Tadashi Watabe ◽  
Yuwei Liu ◽  
Victor Romanov ◽  
Yasukazu Kanai ◽  
...  
Keyword(s):  
Rat Brain ◽  
Cerebral Blood Volume ◽  
Tca Cycle ◽  
Oxygen Metabolism ◽  
Significant Inhibition ◽  
Oxygen Extraction Fraction ◽  
Metabolic Inhibitor ◽  
High Dose ◽  
Cerebral Oxygen ◽  
Ipsilateral Striatum

Fluorocitrate (FC) is a specific metabolic inhibitor of the tricarboxylic acid (TCA) cycle in astrocytes. The purpose of this study was to evaluate whether inhibition of the astrocyte TCA cycle by FC would affect the oxygen metabolism in the rat brain. At 4 h after the intracranial FC injection, the rats (n = 9) were investigated by 15O-labeled gas PET to measure the cerebral blood flow (CBF), the cerebral metabolic rate of oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral blood volume (CBV). After the 15O-gas PET, the rats were given an intravenous injection of 14C-acetate for autoradiography. 15O-gas PET showed no significant differences in any of the measured parameters between the ipsilateral and contralateral striatum (high dose group: CBF (54.4 ± 8.8 and 55.3 ± 11.6 mL/100 mL/min), CMRO2 (7.0 ± 0.9 and 7.1 ± 1.2 mL/100 mL/min), OEF (72.0 ± 8.9 and 70.8 ± 8.2%), and CBV (4.1 ± 0.8 and 4.2 ± 0.9 mL/100 mL), respectively). In contrast, the 14C-acetate autoradiography revealed a significant inhibition of the astrocyte metabolism in the ipsilateral striatum. The regional cerebral oxygen consumption as well as the hemodynamic parameters were maintained even in the face of inhibition of the astrocyte TCA cycle metabolism in the rat brain.

scholarly journals Effect of supplemental dexmedetomidine in interventional embolism on cerebral oxygen metabolism in patients with intracranial aneurysms

2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110029
Author(s):  
Zhang Guo ◽  
Weiwei Wang ◽  
Dahua Xie ◽  
Ruisheng Lin
Keyword(s):  
Intracranial Aneurysms ◽  
Jugular Vein ◽  
Oxygen Metabolism ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism ◽  
Time Points ◽  
Venous Oxygen Saturation ◽  
Group A ◽  
Group B ◽  
Oxygen Difference

Objective To investigate the effect of supplemental dexmedetomidine in interventional embolism on cerebral oxygen metabolism in patients with intracranial aneurysms. Methods Ninety patients who underwent interventional embolism of intracranial aneurysms were equally divided into Group A and Group B. In Group A, dexmedetomidine was injected intravenously 10 minutes before inducing anesthesia, with a loading dose of 0.6 µg/kg followed by 0.4 µg/kg/hour. Group B received the same amount of normal saline by the same injection method. Heart rate (HR), mean arterial pressure (MAP), arterial–jugular venous oxygen difference [D(a-jv) (O2)], cerebral oxygen extraction [CE (O2)], and intraoperative propofol use were recorded before inducing anesthesia (T0) and at five time points thereafter. Results The amount of propofol in Group A was lower vs Group B. At all five time points after T0, HR, MAP, D(a-jv) (O2), and CE (O2) in Group A were significantly lower vs Group B, with significant differences for jugular venous oxygen saturation (SjvO2) and the oxygen content of the internal jugular vein (CjvO2) between the groups. Conclusion Dexmedetomidine resulted in less intraoperative propofol, lower D(a-jv) (O2) and CE (O2), and improved cerebral oxygen metabolism.

scholarly journals Effect of Chlorpromazine on Cerebral Hemodynamics and Cerebral Oxygen Metabolism in Man

Circulation ◽  
1956 ◽  
Vol 14 (3) ◽  
pp. 380-385 ◽  
Author(s):  
JOHN H. MOYER ◽  
GEORGE MORRIS ◽  
ROBERT PONTIUS ◽  
ROBERT HERSHBERGER ◽  
C. Polk Smith
Keyword(s):  
Oxygen Metabolism ◽  
Cerebral Hemodynamics ◽  
Cerebral Oxygen ◽  
Cerebral Oxygen Metabolism
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