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

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.


2003 ◽  
Vol 23 (7) ◽  
pp. 838-844 ◽  
Author(s):  
Chie Seki ◽  
Jeff Kershaw ◽  
Paule-Joanne Toussaint ◽  
Kenichi Kashikura ◽  
Tetsuya Matsuura ◽  
...  

The authors tested the hypothesis that the oxygen content of brain tissue is negligible by injecting an intracarotid bolus of 15O-labeled tracer into rats. Under the hypothesis, the clearance rates of 15O radioactivity from the brain after injections of both 15O-labeled water (H215O) and 15O-labeled oxyhemoglobin (HbO15O) should be identical. However, the logarithmic slope of the 15O radioactivity curve after HbO15O injection (0.494 ± 0.071 min-1) was steeper than that after H215O injection (0.406 ± 0.038 min−1) ( P<0.001, n = 13), where the time range used in the comparison was between 60 and 120 seconds after the injection. A possible interpretation of this result is that nonmetabolized O15O may dwell in the brain tissue for a finite period of time before it is eventually metabolized or returned to the blood stream unaltered. These findings contradict assumptions made by models currently used to measure cerebral oxygen metabolism.



2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Takashi Temma ◽  
Kazuhiro Koshino ◽  
Tetsuaki Moriguchi ◽  
Jun-ichiro Enmi ◽  
Hidehiro Iida

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.



1991 ◽  
Vol 11 (5) ◽  
pp. 837-844 ◽  
Author(s):  
David A. Carpenter ◽  
Robert L. Grubb ◽  
Lee W. Tempel ◽  
William J. Powers

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.



2021 ◽  
Author(s):  
Michael Germuska ◽  
Rachael C Stickland ◽  
Antonio Maria Chiarelli ◽  
Hannah L Chandler ◽  
Richard G Wise

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.



2017 ◽  
Author(s):  
Giri P. Krishnan ◽  
Oscar C. González ◽  
Maxim Bazhenov

AbstractResting or baseline state low frequency (0.01-0.2 Hz) brain activity has been observed in fMRI, EEG and LFP recordings. These fluctuations were found to be correlated across brain regions, and are thought to reflect neuronal activity fluctuations between functionally connected areas of the brain. However, the origin of these infra-slow fluctuations remains unknown. Here, using a detailed computational model of the brain network, we show that spontaneous infra-slow (< 0.05 Hz) fluctuations could originate due to the ion concentration dynamics. The computational model implemented dynamics for intra and extracellular K+ and Na+ and intracellular Cl- ions, Na+/K+ exchange pump, and KCC2 co-transporter. In the network model representing resting awake-like brain state, we observed slow fluctuations in the extracellular K+ concentration, Na+/K+ pump activation, firing rate of neurons and local field potentials. Holding K+ concentration constant prevented generation of these fluctuations. The amplitude and peak frequency of this activity were modulated by Na+/K+ pump, AMPA/GABA synaptic currents and glial properties. Further, in a large-scale network with long-range connections based on CoCoMac connectivity data, the infra-slow fluctuations became synchronized among remote clusters similar to the resting-state networks observed in vivo. Overall, our study proposes that ion concentration dynamics mediated by neuronal and glial activity may contribute to the generation of very slow spontaneous fluctuations of brain activity that are observed as the resting-state fluctuations in fMRI and EEG recordings.



2017 ◽  
Vol 23 (9-10) ◽  
pp. 741-754 ◽  
Author(s):  
Nina F. Dronkers ◽  
Maria V. Ivanova ◽  
Juliana V. Baldo

AbstractStudies of language disorders have shaped our understanding of brain–language relationships over the last two centuries. This article provides a review of this research and how our thinking has changed over the years regarding how the brain processes language. In the 19th century, a series of famous case studies linked distinct speech and language functions to specific portions of the left hemisphere of the brain, regions that later came to be known as Broca’s and Wernicke’s areas. One hundred years later, the emergence of new brain imaging tools allowed for the visualization of brain injuriesin vivothat ushered in a new era of brain-behavior research and greatly expanded our understanding of the neural processes of language. Toward the end of the 20th century, sophisticated neuroimaging approaches allowed for the visualization of both structural and functional brain activity associated with language processing in both healthy individuals and in those with language disturbance. More recently, language is thought to be mediated by a much broader expanse of neural networks that covers a large number of cortical and subcortical regions and their interconnecting fiber pathways. Injury to both grey and white matter has been seen to affect the complexities of language in unique ways that have altered how we think about brain–language relationships. The findings that support this paradigm shift are described here along with the methodologies that helped to discover them, with some final thoughts on future directions, techniques, and treatment interventions for those with communication impairments. (JINS, 2017,23, 741–754)



Author(s):  
V. A. Maksimenko ◽  
A. A. Harchenko ◽  
A. Lüttjohann

Introduction: Now the great interest in studying the brain activity based on detection of oscillatory patterns on the recorded data of electrical neuronal activity (electroencephalograms) is associated with the possibility of developing brain-computer interfaces. Braincomputer interfaces are based on the real-time detection of characteristic patterns on electroencephalograms and their transformation  into commands for controlling external devices. One of the important areas of the brain-computer interfaces application is the control of the pathological activity of the brain. This is in demand for epilepsy patients, who do not respond to drug treatment.Purpose: A technique for detecting the characteristic patterns of neural activity preceding the occurrence of epileptic seizures.Results:Using multi-channel electroencephalograms, we consider the dynamics of thalamo-cortical brain network, preceded the occurrence of an epileptic seizure. We have developed technique which allows to predict the occurrence of an epileptic seizure. The technique has been implemented in a brain-computer interface, which has been tested in-vivo on the animal model of absence epilepsy.Practical relevance:The results of our study demonstrate the possibility of epileptic seizures prediction based on multichannel electroencephalograms. The obtained results can be used in the development of neurointerfaces for the prediction and prevention of seizures of various types of epilepsy in humans. 



2021 ◽  
Vol 49 (4) ◽  
pp. 030006052110029
Author(s):  
Zhang Guo ◽  
Weiwei Wang ◽  
Dahua Xie ◽  
Ruisheng Lin

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.



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