Cerebral glucose metabolism during 30 minutes of moderate hypoxia and reoxygenation

1983 ◽  
Vol 245 (4) ◽  
pp. E365-E372
Author(s):  
D. Kintner ◽  
J. H. Fitzpatrick ◽  
J. A. Louie ◽  
D. D. Gilboe
Keyword(s):  
Glycolytic Flux ◽  
Oxygen Utilization ◽  
Lactate Oxidation ◽  
Cerebral Metabolic Rate ◽  
Show Evidence ◽  
Significant Release ◽  
Lactate Formation ◽  
Metabolite Synthesis ◽  
Posthypoxic Period ◽  
The Brain

In 50 separate experiments, isolated canine brain preparations were subjected to 15 or 30 min of either PaO2 30 mmHg or PaO2 40 mmHg perfusion followed by up to 60 min of reoxygenation at a normal PaO2. The cerebral metabolic rate for glucose (CMRGlu) increased 70-80% after 2 min of hypoxia but then returned to nearly the normal rate by the end of the 30-min period of hypoxia. Glycolytic flux appeared to be facilitated in both groups initially but was inhibited as the hypoxic period continued. This slowing of glycolysis after 15 or 30 min of hypoxia appears to be modulated by the regulatory enzyme phosphofructokinase. Glucose equivalents metabolized, based on CMRGlu plus brain glucose and glycogen disappearance, far exceed the glucose equivalents that can be accounted for on the basis of oxygen utilization and brain lactate formation. Thus, during hypoxia, some of the glucose equivalents must be utilized for synthesis of other metabolites. The glycolytic intermediates returned to normal after reoxygenation in the PaO2 40 mmHg preparations, but the PaO2 30 mmHg preparations continued to show evidence of decreased glycolysis and a lingering lactacidosis. Although posthypoxic oxygen uptake was sufficient to oxidize all glucose entering the brain, there was no significant release of accumulated lactate into the blood. Thus, the decrease in brain tissue lactate must have been the result of lactate oxidation. A significant amount of the glucose entering the brain during the posthypoxic period appears to be used for metabolite synthesis rather than energy production.

scholarly journals Glycolysis versus TCA Cycle in the Primate Brain as Measured by Combining 18F-FDG PET and 13C-NMR

2005 ◽  
Vol 25 (11) ◽  
pp. 1418-1423 ◽  
Author(s):  
Fawzi Boumezbeur ◽  
Laurent Besret ◽  
Julien Valette ◽  
Marie-Claude Gregoire ◽  
Thierry Delzescaux ◽  
...  
Keyword(s):  
Tca Cycle ◽  
Glycolytic Flux ◽  
Cerebral Metabolic Rate ◽  
Metabolic Coupling ◽  
Primate Brain ◽  
Positron Emission ◽  
The Tca Cycle ◽  
The Brain ◽  
Good Agreement ◽  
C Nmr

The glycolytic flux (cerebral metabolic rate of glucose CMRglc) and the TCA cycle flux ( VTCA) were measured in the same monkeys by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) and 13C NMR spectroscopy, respectively. Registration of nuclear magnetic resonance (NMR) and PET data were used for comparison of CMRglc and VTCA in the exact same area of the brain. Both fluxes were in good agreement with literature values (CMR glc 0.23 ± 0.03 μmol/g min, VTCA = 0.53 ± 0.13 μmol/gmin). The resulting [ CMRglc/VTCA] ratio was 0.46 ± 0.12 ( n = 5, mean ± s.d.), not significantly different from the 0.5 expected when glucose is the sole fuel that is completely oxidized. Our results provide a cross-validation of both techniques. Comparison of CMRglc with VTCA is in agreement with a metabolic coupling between the TCA cycle and glycolysis under normal physiologic conditions.

Anoxia and adenosine induce increased cerebral blood flow rate in crucian carp

1994 ◽  
Vol 267 (2) ◽  
pp. R590-R595 ◽  
Author(s):  
G. E. Nilsson ◽  
P. Hylland ◽  
C. O. Lofman
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Crucian Carp ◽  
Blood Flow Rate ◽  
Fold Increase ◽  
Liver Glycogen ◽  
Glycolytic Flux ◽  
Brain Blood Flow ◽  
Atp Production ◽  
The Brain

The crucian carp (Carassius carassius) has the rare ability to survive prolonged anoxia, indicating an extraordinary capacity for glycolytic ATP production, especially in a highly energy-consuming organ like the brain. For the brain to be able to increase its glycolytic flux during anoxia and profit from the large liver glycogen store, an increased glucose delivery from the blood would be expected. Nevertheless, the effect of anoxia on brain blood flow in crucian carp has never been studied previously. We have used epireflection microscopy to directly observe and measure blood flow rate on the brain surface (optic lobes) during normoxia and anoxia in crucian carp. We have also examined the possibility that adenosine participates in the regulation of brain blood flow rate in crucian carp. The results showed a 2.16-fold increase in brain blood flow rate during anoxia. A similar increase was seen after topical application of adenosine during normoxia, while adenosine was without effect during anoxia. Moreover, superfusing the brain with the adenosine receptor blocker aminophylline inhibited the effect of anoxia on brain blood flow rate, clearly suggesting a mediatory role of adenosine in the anoxia-induced increase in brain blood flow rate.

Abstract 2381: Aneurysmal Subarachnoid Hemorrhage: Metabolic and Blood Flow Patterns

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
parham moftakhar ◽  
Thomas C Glenn ◽  
John Boscardin ◽  
Neil A Martin
Keyword(s):  
Blood Flow ◽  
Phase Ii ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Phase Iii ◽  
Entire Study ◽  
Cerebral Metabolic Rate ◽  
Study Population ◽  
Blood Flow Patterns ◽  
The Brain ◽  
Oxygen Difference

Objective: The purpose of this study is to classify and describe the clinically distinct metabolic and hemodynamic phases post-ASAH. Methods: 224 patients who suffered an ASAH (mean age 55±14; 74% female, 26% male) were examined. Patients underwent daily transcranial Doppler (TCD) and cerebral blood flow (CBF) studies (using 133 Xe clearance). Due to the paucity of data on post-hemorrhage day (PHD) 0, the internal carotid artery end-diastolic (ICA ED ) velocity, a surrogate for CBF, was used for the first 24 hours. The brain arteriovenous oxygen difference (AVDO 2 ) was recorded for each patient and the cerebral metabolic rate of oxygen (CMRO 2 ) was calculated. Clinical outcome was evaluated based on the Glasgow Outcome Scale (GOS) 6 months after rupture. Results: Following ASAH, 3 distinct hemodynamic phases arose for the entire study population. Phase I (hypoperfusion phase), occurs on the day of rupture (PHD 0) and is defined by a low ICA ED velocity (mean 17.8±1.1 cm/s), normal middle cerebral artery (MCA) velocity (mean V MCA 58.0±23.4 cm/s), and normal Lindegaard Ratio ([LR], mean 1.66±0.50). Phase II (relative hyperemia), (PHD 1–3), is characterized by an increasing ICA ED (mean 35.4±1.0 cm/s, p<0.0001), a relative hyperemia (mean CBF 15 40.1±1.5 ml/100g/minute, CMRO 2 1.17±0.41 ml/100g/min), a rising V MCA (mean 71.5±5.8 cm/sec, p<0.0001), and a rising but normal LR (mean 2.21±0.19, p<0.0001). During phase III (vasospasm phase, PHD 4–21), both the ICA ED and CBF decrease (mean ICA ED 19.9±0.9 cm/s, p<0.0001; mean CBF 15 36.8±0.7 ml/100g/minute, p=0.04), V MCA continues to rise (mean 107.6±2.9cm/sec, p<0.0001), and the LR is further increased (mean 3.25±0.08, p<0.0001). The CMRO 2 remains low (mean 1.17±0.40 ml/100g/min, p=1). Based on the GOS up to 90% of patients who experienced either a relative or absolute hyperemia had good outcomes. Conclusions: After an ASAH, 3 discrete metabolic and hemodynamic phases arise each with the potential for its own unique phase-specific management and therapy. Relative hyperemia, or “luxury perfusion,” during Phase II in the setting of non-elevated ICPs may provide some type of benefit for patients.

Capturing the Forest but Missing the Trees: Microstates Inadequate for Characterizing Shorter-Scale EEG Dynamics

2019 ◽  
Vol 31 (11) ◽  
pp. 2177-2211 ◽  
Author(s):  
Saurabh Bhaskar Shaw ◽  
Kiret Dhindsa ◽  
James P. Reilly ◽  
Suzanna Becker
Keyword(s):  
Systems Analysis ◽  
Temporal Dynamics ◽  
Field Potential ◽  
Stable States ◽  
Dynamical Systems Analysis ◽  
Eeg Data ◽  
Show Evidence ◽  
Winner Takes All ◽  
Microstate Analysis ◽  
The Brain

The brain is known to be active even when not performing any overt cognitive tasks, and often it engages in involuntary mind wandering. This resting state has been extensively characterized in terms of fMRI-derived brain networks. However, an alternate method has recently gained popularity: EEG microstate analysis. Proponents of microstates postulate that the brain discontinuously switches between four quasi-stable states defined by specific EEG scalp topologies at peaks in the global field potential (GFP). These microstates are thought to be “atoms of thought,” involved with visual, auditory, salience, and attention processing. However, this method makes some major assumptions by excluding EEG data outside the GFP peaks and then clustering the EEG scalp topologies at the GFP peaks, assuming that only one microstate is active at any given time. This study explores the evidence surrounding these assumptions by studying the temporal dynamics of microstates and its clustering space using tools from dynamical systems analysis, fractal, and chaos theory to highlight the shortcomings in microstate analysis. The results show evidence of complex and chaotic EEG dynamics outside the GFP peaks, which is being missed by microstate analysis. Furthermore, the winner-takes-all approach of only one microstate being active at a time is found to be inadequate since the dynamic EEG scalp topology does not always resemble that of the assigned microstate, and there is competition among the different microstate classes. Finally, clustering space analysis shows that the four microstates do not cluster into four distinct and separable clusters. Taken collectively, these results show that the discontinuous description of EEG microstates is inadequate when looking at nonstationary short-scale EEG dynamics.

Ketogenic Diet, Aging, and Neurodegeneration

2016 ◽  
Author(s):  
Kui Xu ◽  
Joseph C. LaManna ◽  
Michelle A. Puchowicz
Keyword(s):  
Oxidative Stress ◽  
Energy Source ◽  
Blood Flow ◽  
Ketogenic Diet ◽  
Ketone Bodies ◽  
Neurovascular Unit ◽  
Cerebral Metabolic Rate ◽  
Downstream Effects ◽  
Atp Supply ◽  
The Brain

The brain is normally completely dependent on glucose, but is capable of using ketones as an alternate energy source, as occurs with prolonged starvation or chronic feeding of a ketogenic diet. Research has shown that ketosis is neuroprotective against ischemic insults in rodents. This review focuses on investigating the mechanistic links to neuroprotection by ketosis in the aged. Recovery from stroke and other pathophysiological conditions in the aged is challenging. Cerebral metabolic rate for glucose, cerebral blood flow, and the defenses against oxidative stress are known to decline with age, suggesting dysfunction of the neurovascular unit. One mechanism of neuroprotection by ketosis involves succinate-induced stabilization of hypoxic inducible factor-1alpha (HIF1α‎) and its downstream effects on intermediary metabolism. The chapter hypothesizes that ketone bodies play a role in the restoration of energy balance (stabilization of ATP supply) and act as signaling molecules through the up-regulation of salvation pathways targeted by HIF1α‎.

Effect of anterior and posterior hypothalamic lesions on precocious sexual maturation

1964 ◽  
Vol 206 (4) ◽  
pp. 805-810 ◽  
Author(s):  
Raul C. Schiavi
Keyword(s):  
Sexual Maturation ◽  
Female Rats ◽  
Vaginal Opening ◽  
Uterine Weight ◽  
Comparative Effect ◽  
Hypothalamic Lesions ◽  
Medial Hypothalamus ◽  
Show Evidence ◽  
The Brain ◽  
Made In

The comparative effect of anterior and posterior hypothalamic lesions on the development of sexual maturation of prepubertal female rats was investigated. Lesions by electrocoagulation were made in the medial hypothalamus of 45 rats at 25–26 days of age. Thirty-nine animals of the same age constituted the sham-operated and nonoperated controls. A hastened appearance of vaginal opening and first estrus, a significant increase in uterine weight, precocious ovarian luteinization, and premature sexual cycles were observed following both types of lesions. Sham-operated rats and animals with lesions in other parts of the brain did not show evidence of precocious sexual maturation.

Magnetic resonance cerebral metabolic rate of oxygen utilization in hyperacute stroke patients

2003 ◽  
Vol 53 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Jin-Moo Lee ◽  
Katie D. Vo ◽  
Hongyu An ◽  
Azim Celik ◽  
Yueh Lee ◽  
...  
Keyword(s):  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Oxygen Utilization ◽  
Stroke Patients ◽  
Hyperacute Stroke ◽  
Cerebral Metabolic Rate

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.

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