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 Cerebral metabolic rate of oxygen during transition from wakefulness to sleep measured with high temporal resolution OxFlow MRI with concurrent EEG

2020 ◽  
pp. 0271678X2091928
Author(s):  
Alessandra Caporale ◽  
Hyunyeol Lee ◽  
Hui Lei ◽  
Hengyi Rao ◽  
Michael C Langham ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Cerebral Metabolism ◽  
Sleep Onset ◽  
High Temporal Resolution ◽  
Mean Values ◽  
Cerebral Metabolic Rate ◽  
Sleep Physiology ◽  
Concomitant Reduction

During slow-wave sleep, synaptic transmissions are reduced with a concomitant reduction in brain energy consumption. We used 3 Tesla MRI to noninvasively quantify changes in the cerebral metabolic rate of O2 (CMRO2) during wakefulness and sleep, leveraging the ‘OxFlow’ method, which provides venous O2 saturation (SvO2) along with cerebral blood flow (CBF). Twelve healthy subjects (31.3 ± 5.6 years, eight males) underwent 45–60 min of continuous scanning during wakefulness and sleep, yielding one image set every 3.4 s. Concurrent electroencephalography (EEG) data were available in eight subjects. Mean values of the metabolic parameters measured during wakefulness were stable, with coefficients of variation below 7% (average values: CMRO2 = 118 ± 12 µmol O2/min/100 g, SvO2 = 67.0 ± 3.7% HbO2, CBF = 50.6 ±4.3 ml/min/100 g). During sleep, on average, CMRO2 decreased 21% (range: 14%–32%; average nadir = 98 ± 16 µmol O2/min/100 g), while EEG slow-wave activity, expressed in terms of [Formula: see text]-power, increased commensurately. Following sleep onset, CMRO2 was found to correlate negatively with relative [Formula: see text]-power (r = −0.6 to −0.8, P < 0.005), and positively with heart rate (r = 0.5 to 0.8, P < 0.0005). The data demonstrate that OxFlow MRI can noninvasively measure dynamic changes in cerebral metabolism associated with sleep, which should open new opportunities to study sleep physiology in health and disease.

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 Overview of Monitoring of Cerebral Blood Flow and Metabolism after Severe Head Injury

1994 ◽  
Vol 21 (S1) ◽  
pp. S6-S11 ◽  
Author(s):  
J. Paul Muizelaar ◽  
Marc L. Schröder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Severe Head Injury ◽  
Cerebral Metabolism ◽  
Jugular Bulb ◽  
Cerebral Metabolic Rate ◽  
Venous Oxygen Saturation ◽  
Arteriovenous Difference ◽  
The Brain ◽  
Pressure Autoregulation

AbstractThe relationships between cerebral blood flow (CBF), cerebral metabolism (cerebral metabolic rate of oxygen, CMRO2) and cerebral oxygen extraction (arteriovenous difference of oxygen, AVDO2) are discussed, using the formula CMRO2 = CBF × AVDO2. Metabolic autoregulation, pressure autoregulation and viscosity autoregulation can all be explained by the strong tendency of the brain to keep AVDO2 constant. Monitoring of CBF, CMRO2 or AVDO2 very early after injury is impractical, but the available data indicate that cerebral ischemia plays a considerable role at this stage. It can best be avoided by not "treating" arterial hypertension and not using too much hyperventilation, while generous use of mannitol is probably beneficial. Once in the ICU, treatment can most practically be guided by monitoring of jugular bulb venous oxygen saturation. If saturation drops below 50%, the reason for this must be found (high intracranial pressure, blood pressure not high enough, too vigorous hyperventilation, arterial hypoxia, anemia) and must be treated accordingly.

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 Rapid magnetic resonance measurement of global cerebral metabolic rate of oxygen consumption in humans during rest and hypercapnia

2011 ◽  
Vol 31 (7) ◽  
pp. 1504-1512 ◽  
Author(s):  
Varsha Jain ◽  
Michael C Langham ◽  
Thomas F Floyd ◽  
Gaurav Jain ◽  
Jeremy F Magland ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Consumption ◽  
Magnetic Resonance ◽  
Metabolic Rate ◽  
Vascular Reactivity ◽  
Cerebral Metabolism ◽  
Metabolic Effects ◽  
Cerebral Metabolic Rate ◽  
Rate Of Oxygen Consumption ◽  
End Tidal

The effect of hypercapnia on cerebral metabolic rate of oxygen consumption ( CMRO2) has been a subject of intensive investigation and debate. Most applications of hypercapnia are based on the assumption that a mild increase in partial pressure of carbon dioxide has negligible effect on cerebral metabolism. In this study, we sought to further investigate the vascular and metabolic effects of hypercapnia by simultaneously measuring global venous oxygen saturation ( Sv O2) and total cerebral blood flow ( tCBF), with a temporal resolution of 30 seconds using magnetic resonance susceptometry and phase-contrast techniques in 10 healthy awake adults. While significant increases in Sv O2 and tCBF were observed during hypercapnia ( P < 0.005), no change in CMRO2 was noted ( P > 0.05). Additionally, fractional changes in tCBF and end-tidal carbon dioxide ( R2 = 0.72, P < 0.005), as well as baseline Sv O2 and tCBF ( R2 = 0.72, P < 0.005), were found to be correlated. The data also suggested a correlation between cerebral vascular reactivity ( CVR) and baseline tCBF ( R2 = 0.44, P = 0.052). A CVR value of 6.1% ± 1.6%/mm Hg was determined using a linear-fit model. Additionally, an average undershoot of 6.7% ± 4% and 17.1% ± 7% was observed in Sv O2 and tCBF upon recovery from hypercapnia in six subjects.

scholarly journals Changes in regional cerebral metabolism during systemic hyperthermia in humans

2002 ◽  
Vol 92 (2) ◽  
pp. 846-851 ◽  
Author(s):  
Sarah A. Nunneley ◽  
Charles C. Martin ◽  
James W. Slauson ◽  
Christopher M. Hearon ◽  
Lisa D. H. Nickerson ◽  
...  
Keyword(s):  
Metabolic Rate ◽  
Cerebral Metabolism ◽  
Human Subjects ◽  
Resting Metabolic Rate ◽  
Brain Regions ◽  
Hot Water ◽  
Whole Body ◽  
Cerebral Metabolic Rate ◽  
Positron Emission ◽  
Systemic Responses

Whole body hyperthermia may produce vasodialation, nausea, and altered cognitive function. Animal research has identified brain regions that have important roles in thermoregulation. However, differences in both the cognitive and sweating abilities of humans and animals implicate the need for human research. Positron emission tomography (PET) was used to identify brain regions with altered activity during systemic hyperthermia. Human subjects were studied under cool (control) conditions and during steady-state hyperthermia induced by means of a liquid-conditioned suit perfused with hot water. PET images were obtained by injecting [18F]fluorodeoxyglucose, waiting 20 min for brain uptake, and then scanning for 10 min. Heating was associated with a 23% increase in resting metabolic rate. Significant increases in cerebral metabolic rate occurred in the hypothalamus, thalamus, corpus callosum, cingulate gyrus, and cerebellum. In contrast, significant decreases occurred in the caudate, putamen, insula, and posterior cingulum. These results are important for understanding the mechanisms responsible for altered cognitive and systemic responses during hyperthermia. Novel regions (e.g., lateral cerebellum) with possible thermoregulatory roles were identified.

Effects of hyperthermia on cerebral blood flow and metabolism during prolonged exercise in humans

2002 ◽  
Vol 93 (1) ◽  
pp. 58-64 ◽  
Author(s):  
Lars Nybo ◽  
Kirsten Møller ◽  
Stefanos Volianitis ◽  
Bodil Nielsen ◽  
Niels H. Secher
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Metabolic Rate ◽  
Core Temperature ◽  
Prolonged Exercise ◽  
Cerebral Metabolism ◽  
Cycle Ergometer ◽  
Carbon Dioxide Tension ◽  
Cerebral Metabolic Rate ◽  
Exercise In Humans

The development of hyperthermia during prolonged exercise in humans is associated with various changes in the brain, but it is not known whether the cerebral metabolism or the global cerebral blood flow (gCBF) is affected. Eight endurance-trained subjects completed two exercise bouts on a cycle ergometer. The gCBF and cerebral metabolic rates of oxygen, glucose, and lactate were determined with the Kety-Schmidt technique after 15 min of exercise when core temperature was similar across trials, and at the end of exercise, either when subjects remained normothermic (core temperature = 37.9°C; control) or when severe hyperthermia had developed (core temperature = 39.5°C; hyperthermia). The gCBF was similar after 15 min in the two trials, and it remained stable throughout control. In contrast, during hyperthermia gCBF decreased by 18% and was therefore lower in hyperthermia compared with control at the end of exercise (43 ± 4 vs. 51 ± 4 ml · 100 g−1· min−1; P < 0.05). Concomitant with the reduction in gCBF, there was a proportionally larger increase in the arteriovenous differences for oxygen and glucose, and the cerebral metabolic rate was therefore higher at the end of the hyperthermic trial compared with control. The hyperthermia-induced lowering of gCBF did not alter cerebral lactate release. The hyperthermia-induced reduction in exercise cerebral blood flow seems to relate to a concomitant 18% lowering of arterial carbon dioxide tension, whereas the higher cerebral metabolic rate of oxygen may be ascribed to a Q10(temperature) effect and/or the level of cerebral neuronal activity associated with increased exertion.

scholarly journals Neural regulation of hypoxia-inducible factors and redox state drives the pathogenesis of hypertension in a rodent model of sleep apnea

2015 ◽  
Vol 119 (10) ◽  
pp. 1152-1156 ◽  
Author(s):  
Gregg L. Semenza ◽  
Nanduri R. Prabhakar
Keyword(s):  
Nervous System ◽  
Sleep Apnea ◽  
Sympathetic Nervous System ◽  
Brain Stem ◽  
Carotid Body ◽  
Sympathetic Neurons ◽  
Ventrolateral Medulla ◽  
Obstructive Sleep ◽  
Sympathetic Nervous ◽  
The Brain

Obstructive sleep apnea (OSA) is one of the most common causes of hypertension in western societies. OSA causes chronic intermittent hypoxia (CIH) in specialized O2-sensing glomus cells of the carotid body. CIH generates increased reactive oxygen species (ROS) that trigger a feedforward mechanism in which increased intracellular calcium levels ([Ca2+]i) trigger increased HIF-1α synthesis and increased HIF-2α degradation. As a result, the normal homeostatic balance between HIF-1α-dependent prooxidant and HIF-2α-dependent antioxidant enzymes is disrupted, leading to further increases in ROS. Carotid body sensory nerves project to the nucleus tractus solitarii, from which the information is relayed via interneurons to the rostral ventrolateral medulla in the brain stem, which sends sympathetic neurons to the adrenal medulla to stimulate the release of epinephrine and norepinephrine, catecholamines that increase blood pressure. At each synapse, neurotransmitters trigger increased [Ca2+]i, HIF-1α:HIF-2α, and Nox2:Sod2 activity that generates increased ROS levels. These responses are not observed in other regions of the brain stem that do not receive input from the carotid body or signal to the sympathetic nervous system. Thus sympathetic nervous system homeostasis is dependent on a balance between HIF-1α and HIF-2α, disruption of which results in hypertension in OSA patients.

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.

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