scholarly journals Hyperammonaemia depresses glucose consumption throughout the brain

1991 ◽  
Vol 277 (3) ◽  
pp. 693-696 ◽  
Author(s):  
J Jessy ◽  
M R DeJoseph ◽  
R A Hawkins
Keyword(s):  
Hepatic Encephalopathy ◽  
Metabolic Rate ◽  
Brain Function ◽  
Inverse Correlation ◽  
Glucose Consumption ◽  
Brain Structures ◽  
High Plasma ◽  
Plasma Ammonia ◽  
Cerebral Metabolic Rate ◽  
The Brain

Recent studies showed that hyperammonaemia caused many of the metabolic changes in portacaval-shunted rats, a model of hepatic encephalopathy. These changes included a depression in the cerebral metabolic rate of glucose (CMRGlc), an indication of decreased brain function. 2. The purpose of the present experiments was to determine whether the depression of CMRGlc caused by ammonia is confined to certain brain structures, or whether the depression is an overall decrease in all structures, such as occurs in portacaval-shunted rats. To accomplish this objective, rats were made hyperammonaemic by giving them intraperitoneal injections of 40 units of urease/kg body wt. every 12 h; control rats received 0.154 m-NaCl. CMRGlc was measured 48 h after the first injection, by using quantitative autoradiography with [6-14C]glucose as a tracer. 3. The experimental rats had high plasma ammonia concentrations (control 70 nmol/ml, experimental 610 nmol/ml) and brain glutamine levels (control 5.4 mumol/ml). Hyperammonaemia decreased CMRGlc throughout the brain by an average of 19%. CMRGlc showed an inverse correlation with plasma ammonia, but a stronger correlation with the brain glutamine content. 4. Hyperammonaemia led to a decrease in CMRGlc throughout the brain that was indistinguishable from the pattern seen in portacaval-shunted rats. This is taken as further evidence that the cerebral depression found in portacaval-shunted rats is a consequence of hyperammonaemia. The observation that depression of CMRGlc correlated more closely with brain glutamine content than with plasma ammonia suggests that metabolism of ammonia is an important step in the pathological sequence.

Glucose consumption decreases throughout the brain only hours after portacaval shunting

1991 ◽  
Vol 260 (4) ◽  
pp. E613-E619
Author(s):  
M. R. DeJoseph ◽  
R. A. Hawkins
Keyword(s):  
Hepatic Encephalopathy ◽  
Portacaval Shunt ◽  
Glucose Consumption ◽  
Brain Cells ◽  
Cerebral Metabolic Rate ◽  
A Value ◽  
Portacaval Shunting ◽  
Cerebral Dysfunction ◽  
Autoradiographic Technique ◽  
The Brain

The cerebral metabolic rate for glucose (CMRGlc) was measured at the level of individual structures 6, 12, 24, and 48 h and 4 wk after the formation of a portacaval shunt in rats, a model of hepatic encephalopathy. A quantitative autoradiographic technique with [6-14C]glucose as tracer was used. After 6 h, CMRGlc was depressed in all areas measured by an average of 16%. By 48 h, CMRGlc fell further and reached a value comparable to that seen in rats shunted for many weeks (25-30% below normal). The decrease in CMRGlc occurred throughout the brain to about the same degree. CMRGlc was also measured with another tracer, deoxy-D-[14C]glucose, 48 h after portacaval shunting. The deoxy-D-glucose results agreed with those obtained with [6-14C]glucose. The decrease in CMRGlc may be interpreted to be a consequence of the decreased activity of brain cells, reflecting the cerebral dysfunction that occurs when liver function is inadequate. The experiments demonstrate that the onset of cerebral dysfunction occurs within hours of portacaval shunting and is fully established within days.

Delirium: Phenomenology and Diagnosis—A Neurobiologic View

1991 ◽  
Vol 3 (2) ◽  
pp. 121-134 ◽  
Author(s):  
John P. Blass ◽  
Karen A. Nolan ◽  
Ronald S. Black ◽  
Akira Kurita
Keyword(s):  
Differential Diagnosis ◽  
Metabolic Rate ◽  
Functional Impairment ◽  
Cortical Neurons ◽  
Brain Diseases ◽  
Subcortical Structures ◽  
Confusional State ◽  
Cerebral Metabolic Rate ◽  
Neuronal Metabolism ◽  
The Brain

“Delirium” is a reversible confusional state. It results from widespread but reversible interference with the function of cortical neurons, as documented by diffuse slowing on EEG and decreases in cerebral metabolic rate. Delirium can be due to impairments in neuronal metabolism, in neurotransmission (notably cholinergic), or in input from subcortical structures. Engel and Romano (1959) formulated delirium and dementia as the two poles of a spectrum of “cerebral insufficiency,” with delirium resulting from reversible functional impairment and dementia from irreversible anatomic damage. So many disorders can precipitate delirium that the differential diagnosis tests every facet of one's knowledge of medicine. With aging, both normative changes in the brain and the increasing incidence of brain diseases predispose to the development of delirium. The brain damage responsible for a dementia can sensitize to the development of a superimposed delirium.

scholarly journals New Molecular Knowledge Towards the Trigemino-Cardiac Reflex as a Cerebral Oxygen-Conserving Reflex

2010 ◽  
Vol 10 ◽  
pp. 811-817 ◽  
Author(s):  
N. Sandu ◽  
T. Spiriev ◽  
F. Lemaitre ◽  
A. Filis ◽  
B. Schaller
Keyword(s):  
Metabolic Rate ◽  
Cerebral Metabolism ◽  
Sympathetic Neurons ◽  
Small Population ◽  
Molecular Organization ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Cerebral Metabolic Rate ◽  
External Stimuli ◽  
The Brain

The trigemino-cardiac reflex (TCR) represents the most powerful of the autonomous reflexes and is a subphenomenon in the group of the so-called “oxygen-conserving reflexes”. Within seconds after the initiation of such a reflex, there is a powerful and differentiated activation of the sympathetic system with subsequent elevation in regional cerebral blood flow (CBF), with no changes in the cerebral metabolic rate of oxygen (CMRO2) or in the cerebral metabolic rate of glucose (CMRglc). Such an increase in regional CBF without a change of CMRO2or CMRglcprovides the brain with oxygen rapidly and efficiently. Features of the reflex have been discovered during skull base surgery, mediating reflex protection projects via currently undefined pathways from the rostral ventrolateral medulla oblongata to the upper brainstem and/or thalamus, which finally engage a small population of neurons in the cortex. This cortical center appears to be dedicated to transduce a neuronal signal reflexively into cerebral vasodilatation and synchronization of electrocortical activity; a fact that seems to be unique among autonomous reflexes. Sympathetic excitation is mediated by cortical-spinal projection to spinal preganglionic sympathetic neurons, whereas bradycardia is mediated via projections to cardiovagal motor medullary neurons. The integrated reflex response serves to redistribute blood from viscera to the brain in response to a challenge to cerebral metabolism, but seems also to initiate a preconditioning mechanism. Previous studies showed a great variability in the human TCR response, in special to external stimuli and individual factors. The TCR gives, therefore, not only new insights into novel therapeutic options for a range of disorders characterized by neuronal death, but also into the cortical and molecular organization of the brain.

scholarly journals Hyperammonaemia does not impair brain function in the absence of net glutamine synthesis

1991 ◽  
Vol 277 (3) ◽  
pp. 697-703 ◽  
Author(s):  
R A Hawkins ◽  
J Jessy
Keyword(s):  
Amino Acids ◽  
Brain Function ◽  
Aromatic Amino Acids ◽  
Preceding Paper ◽  
Glucose Consumption ◽  
High Energy ◽  
High Energy Phosphates ◽  
Intermediary Metabolites ◽  
Glutamine Synthesis ◽  
The Brain

1. It has been established that chronic hyperammonaemia, whether caused by portacaval shunting or other means, leads to a variety of metabolic changes, including a depression in the cerebral metabolic rate of glucose (CMRGlc) increased permeability of the blood-brain barrier to neutral amino acids, and an increase in the brain content of aromatic amino acids. The preceding paper [Jessy, DeJoseph & Hawkins (1991) Biochem. J. 277, 693-696] showed that the depression in CMRGlc caused by hyperammonaemia correlated more closely with glutamine, a metabolite of ammonia, than with ammonia itself. This suggested that ammonia (NH3 and NH4+) was without effect. The present experiments address the question whether ammonia, in the absence of net glutamine synthesis, induces any of the metabolic symptoms of cerebral dysfunction associated with hyperammonaemia. 2. Small doses of methionine sulphoximine, an inhibitor of glutamine synthetase, were used to raise the plasma ammonia levels of normal rats without increasing the brain glutamine content. These hyperammonaemic rats, with plasma and brain ammonia levels equivalent to those known to depress brain function, behaved normally over 48 h. There was no depression of cerebral energy metabolism (i.e. the rate of glucose consumption). Contents of key intermediary metabolites and high-energy phosphates were normal. Neutral amino acid transport (tryptophan and leucine) and the brain contents of aromatic amino acids were unchanged. 3. The data suggest that ammonia is without effect at concentrations less than 1 mumol/ml if it is not converted into glutamine. The deleterious effect of chronic hyperammonaemia seems to begin with the synthesis of glutamine.

scholarly journals Non-Invasive measurement of the cerebral metabolic rate of oxygen using MRI in rodents

2021 ◽  
Vol 6 ◽  
pp. 109
Author(s):  
Tobias C Wood ◽  
Diana Cash ◽  
Eilidh MacNicol ◽  
Camilla Simmons ◽  
Eugene Kim ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Imaging Techniques ◽  
Glucose Consumption ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Strongly Correlated ◽  
Non Invasive ◽  
Cerebral Metabolic Rate ◽  
Invasive Measurement

Malfunctions of oxygen metabolism are suspected to play a key role in a number of neurological and psychiatric disorders, but this hypothesis cannot be properly investigated without an in-vivo non-invasive measurement of brain oxygen consumption. We present a new way to measure the Cerebral Metabolic Rate of Oxygen (CMRO2) by combining two existing magnetic resonance imaging techniques, namely arterial spin-labelling and oxygen extraction fraction mapping. This method was validated by imaging rats under different anaesthetic regimes and was strongly correlated to glucose consumption measured by autoradiography.

scholarly journals Non-Invasive measurement of the cerebral metabolic rate of oxygen using MRI in rodents

2021 ◽  
Vol 6 ◽  
pp. 109
Author(s):  
Tobias C Wood ◽  
Diana Cash ◽  
Eilidh MacNicol ◽  
Camilla Simmons ◽  
Eugene Kim ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Imaging Techniques ◽  
Glucose Consumption ◽  
Oxygen Metabolism ◽  
Oxygen Extraction Fraction ◽  
Strongly Correlated ◽  
Non Invasive ◽  
Cerebral Metabolic Rate ◽  
Invasive Measurement

Malfunctions of oxygen metabolism are suspected to play a key role in a number of neurological and psychiatric disorders, but this hypothesis cannot be properly investigated without an in-vivo non-invasive measurement of brain oxygen consumption. We present a new way to measure the Cerebral Metabolic Rate of Oxygen (CMRO2) by combining two existing magnetic resonance imaging techniques, namely arterial spin-labelling and oxygen extraction fraction mapping. This method was validated by imaging rats under different anaesthetic regimes and was strongly correlated to glucose consumption measured by autoradiography.

scholarly journals Method for Rapid MRI Quantification of Global Cerebral Metabolic Rate of Oxygen

2015 ◽  
Vol 35 (10) ◽  
pp. 1616-1622 ◽  
Author(s):  
Suliman Barhoum ◽  
Michael C Langham ◽  
Jeremy F Magland ◽  
Zachary B Rodgers ◽  
Cheng Li ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
T Test ◽  
Quantitative Magnetic Resonance Imaging ◽  
Cerebral Metabolic Rate ◽  
Sagittal Sinus ◽  
Scan Time ◽  
Rapid Mri ◽  
Magnetic Resonance Imaging Mri ◽  
The Brain ◽  
Good Agreement

A recently reported quantitative magnetic resonance imaging (MRI) method denoted OxFlow has been shown to be able to quantify whole-brain cerebral metabolic rate of oxygen (CMRO2) by simultaneously measuring oxygen saturation ( S v O 2) in the superior sagittal sinus and cerebral blood flow (CBF) in the arteries feeding the brain in 30 seconds, which is adequate for measurement at baseline but not necessarily in response to neuronal activation. Here, we present an accelerated version of the method (referred to as F-OxFlow) that quantifies CMRO2 in 8 seconds scan time under full retention of the parent method's capabilities and compared it with its predecessor at baseline in 10 healthy subjects. Results indicate excellent agreement between both sequences, with mean bias of 2.2% ( P = 0.18, two-tailed t-test), 3.4% ( P = 0.08, two-tailed t-test), and 2.0% ( P = 0.56, two-tailed t-test) for SvO2, CBF, and CMRO2, respectively. F-OxFlow's potential to monitor dynamic changes in SvO2, CBF, and CMRO2 is illustrated in a paradigm of volitional apnea applied to five of the study subjects. The sequence captured an average increase in SvO2, CBF, and CMRO2 of 10.1 ± 2.5%, 43.2 ± 9.2%, and 7.1 ± 2.2%, respectively, in good agreement with literature values. The method may therefore be suited for monitoring alterations in CBF and SvO2 in response to neurovascular stimuli.

scholarly journals 0424 Effect of Chronic Intermittent Hypoxia on Global Cerebral Metabolic Rate of Oxygen Consumption in Rats

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A162-A163
Author(s):  
J Xu ◽  
E Geng ◽  
L Brake ◽  
A Wiemken ◽  
B Keenan ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Oxygen Consumption ◽  
Sleep Apnea ◽  
Metabolic Rate ◽  
Intermittent Hypoxia ◽  
Sleep Cycle ◽  
Chronic Intermittent Hypoxia ◽  
Cerebral Metabolic Rate ◽  
Obstructive Sleep ◽  
The Brain

Abstract Introduction Patients with obstructive sleep apnea (OSA) commonly exhibit grey and white matter loss, which may be related to hypoxic damage in the brain during sleep. Our preliminary data demonstrated lower values of cerebral metabolic rate of oxygen (CMRO2) consumption in apneics versus controls. As such, reduced CMRO2 may be an important contributor to the neurologic consequences of OSA. Here we report a rodent model for chronic intermittent hypoxia (CIH) to quantify effects on CMRO2 consumption. We hypothesized that increased severity of CIH results in decreased CMRO2 levels. Methods Three groups of rats were subject to varying levels of hypoxia: sham (21% oxygen; n = 19), moderate (11% oxygen; n = 14), and severe (6% oxygen; n = 21). To deliver hypoxia, rats were exposed to three-minute cycles of oxygen between 21% and condition-specific nadir O2 for 12 hours daily during their sleep cycle. CMRO2 values were measured with MRI techniques, performed on anesthetized rats before and after 3 months exposure to CIH. Results Rats from the three hypoxia groups did not differ significantly in CMRO2 values at baseline (0 months). After 3 months of exposure to hypoxic conditions, there was a trending difference (p=0.0726) in percent change from baseline between severely hypoxic (-35.3%) and sham (+12.3%) rats. Moderately hypoxic rats demonstrated an intermediate decrease from baseline after 3 months (-19.0%). Conclusion Our findings suggest that increased severity of intermittent hypoxia yields a dose-response decrease in brain oxygen consumption. Our data add to the growing body of evidence on the relationship between obstructive sleep apnea and hypoxic damage in the brain, suggesting that CMRO2 levels may be an indicator of the neurologic consequences of OSA. Support Funded by NIH P01 HL094307

scholarly journals Striatal and Cortical BOLD, Blood Flow, Blood Volume, Oxygen Consumption, and Glucose Consumption Changes in Noxious Forepaw Electrical Stimulation

2010 ◽  
Vol 31 (3) ◽  
pp. 832-841 ◽  
Author(s):  
Yen-Yu I Shih ◽  
Hsiao-Ying Wey ◽  
Bryan H De La Garza ◽  
Timothy Q Duong
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Metabolic Rate ◽  
Blood Volume ◽  
Functional Imaging ◽  
Cerebral Blood Volume ◽  
Glucose Consumption ◽  
Blood Oxygenation ◽  
Cerebral Metabolic Rate ◽  
Positron Emission

Recent reports showed noxious forepaw stimulation in rats evoked an unexpected sustained decrease in cerebral blood volume (CBV) in the bilateral striatum, whereas increases in spike activity and Fos-immunoreactive cells were observed. This study aimed to further evaluate the hemodynamic and metabolic needs in this model and the sources of negative functional magnetic resonance imaging (fMRI) signals by measuring blood oxygenation-level-dependent (BOLD), cerebral-blood-flow (CBF), CBV, and oxygen-consumption (i.e., cerebral metabolic rate of oxygen (CMRO2)) changes using an 11.7-T MRI scanner, and glucose-consumption (i.e., cerebral metabolic rate of glucose (CMRglc)) changes using micro-positron emission tomography. In the contralateral somatosensory cortex, BOLD, CBF, CBV, CMRO2 ( n=7, P<0.05), and CMRglc ( n=5, P<0.05) increased. In contrast, in the bilateral striatum, BOLD, CBF, and CBV decreased ( P<0.05), CMRO2 decreased slightly, although not significantly from baseline, and CMRglc was not statistically significant from baseline ( P>0.05). These multimodal functional imaging findings corroborate the unexpected negative hemodynamic changes in the striatum during noxious forepaw stimulation, and support the hypothesis that striatal hemodynamic response is dominated by neurotransmitter-mediated vasoconstriction, overriding the stimulus-evoked fMRI signal increases commonly accompany elevated neuronal activity. Multimodal functional imaging approach offers a means to probe the unique attributes of the striatum, providing novel insights into the neurovascular coupling in the striatum. These findings may have strong implications in fMRI studies of pain.

scholarly journals Dependent behavior and the model of family relations in the system of "safe" attachment

2021 ◽  
pp. 44-46
Author(s):  
Svitlana Grygorieva
Keyword(s):  
Significant Interaction ◽  
Family Relations ◽  
Sensory Information ◽  
Inverse Correlation ◽  
Brain Structures ◽  
Significant Inverse Correlation ◽  
Dependent Personality ◽  
Dependent Behavior ◽  
Mother And Child ◽  
The Brain

This article examines a model of family relations, namely the “mother-child” dyad, built on the basis of a study of the lateral profile of normo-typical adolescents and their mothers. Testing the position of postures (comparing the interlacing of the fingers, crossing the arms on the chest, aiming and applauding) revealed a highly significant inverse correlation for the leading eye. This suggests that there is a significant interaction between the structures of the brain of the mother and the child in the thalamus (visual hillocks). The asymmetry of the brain structures of the mother-child dyad indicates their difference in the style of processing sensory information. These differences give rise to the dominance of the pair in the leading hemisphere of the brain (left or right) and, accordingly, in the style of thinking, which does not coincide in this pair. Thus, the state of "reliable" attachment in the mother-child dyad depends on whether the mother is ready to accept a different way of thinking (reading and processing sensory information) in her child. Based on the physiological characteristics of the structure of the brain of the mother and child, we will consider the system of dependent personality behavior, caused by disorders of interaction and attachment.

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