Cerebral blood flow and energy metabolism during stress

Many, but not all, stressful events are accompanied by increases in cerebral blood flow and/or energy metabolism. The stressful events include pharmacological paralysis, footshock, conditioned fear, hypotension, hypoglycemia, hypoxia, noise, and ethanol withdrawal. These increases are significant because 1) all brain regions are often affected, i.e., certain stressful events have global effects on cerebral blood flow and energy metabolism; and 2) various stressful events appear to have a common adrenergic mechanism for increasing cerebral blood flow and energy metabolism. The adrenergic mechanism involves beta-adrenergic receptor stimulation by either epinephrine secreted from the adrenal medulla or possibly norepinephrine endogenous to the brain. While adrenergic mechanisms are not the only mechanism controlling flow and metabolism for a given stressful condition, they do appear to be common to many situations. At least part of the increase in cerebral blood flow and energy metabolism during many conditions appears to be the result of the stress response and not directly a result of the condition itself.

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Relationship between Cardiopulmonary Bypass Flow Rate and Cerebral Embolization in Dogs

Anesthesiology ◽

10.1097/00000542-199911000-00031 ◽

1999 ◽

Vol 91 (5) ◽

pp. 1387-1387 ◽

Cited By ~ 11

Author(s):

Hulya Sungurtekin ◽

Walter Plöchl ◽

David J. Cook

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Cardiopulmonary Bypass ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Rank Order ◽

Brain Regions ◽

Pump Flow ◽

Cerebral Embolization ◽

The Brain

Background Cerebral embolization is a primary cause of cardiac surgical neurologic morbidity. During cardiopulmonary bypass (CPB), there are well-defined periods of embolic risk. In theory, cerebral embolization might be reduced by an increase in pump flow during these periods. The purpose of this study was to determine the CPB flow-embolization relation in a canine model. Methods Twenty mongrel dogs underwent CPB at 35 degrees C with alpha-stat management and a fentanyl-midazolam anesthetic. In each animal, CPB flow was adjusted to achieve a mean arterial pressure of 65-75 mmHg. During CPB, an embolic load of 1.2 x 10(5) 67 microm fluorescent microspheres was injected into the arterial inflow line. Before and after embolization, cerebral blood flow was determined using 15-microm microspheres. Tissue was taken from 12 brain regions and microspheres were recovered. The relation between pump flow and embolization/g of brain was determined. Results The mean arterial pressure at embolization was 67 +/-4 mmHg, and the range of pump flow was 0.9-3.5 l x min(-1)x m(-2). Cerebral blood flow was independent of pump flow. At lower pump flow, the percentage of that flow delivered to the brain increased. There was a strong inverse relation between pump flow and cerebral embolization (r = -0.708, P < 0.000 by Spearman rank order correlation). Conclusions Cerebral embolization is determined by the CPB flow. At an unchanged mean arterial pressure, as pump flow is reduced, a progressively greater proportion of that flow is delivered to the brain.

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Effects of Immobilization Stress on Cerebral Blood Flow and Cerebrovascular Permeability in Spontaneously Hypertensive Rats

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1982.39 ◽

1982 ◽

Vol 2 (3) ◽

pp. 373-379 ◽

Cited By ~ 13

Author(s):

M. Ohata ◽

H. Takei ◽

W. R. Fredericks ◽

S. I. Rapoport

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Spontaneously Hypertensive Rats ◽

Brain Regions ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Brain Barrier Permeability ◽

Cerebrovascular Permeability ◽

Area Product ◽

The Brain

Immobilization of unanesthetized, freely breathing, 10–12-month-old, spontaneously hypertensive rats (SHR) did not significantly alter regional cerebral blood flow (rCBF) in 13 of 14 brain regions assayed. After 5 or 15 min of immobilization, rCBF was unchanged except at the frontal lobe, where it rose significantly by 21%. Furthermore, immobilization did not increase the cerebrovascular permeability–area product for 14C-sucrose, except at three brain regions. The results indicate that immobilization of SHR does not significantly affect rCBF or blood–brain barrier permeability in most regions of the brain, and suggest that adequate autoregulation of rCBF is maintained under stress.

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Response of Cerebral Blood Flow and Blood Pressure to Dynamic Exercise: A Study Using PET

International Journal of Sports Medicine ◽

10.1055/s-0043-123647 ◽

2018 ◽

Vol 39 (03) ◽

pp. 181-188 ◽

Cited By ~ 3

Author(s):

Mikio Hiura ◽

Tadashi Nariai ◽

Muneyuki Sakata ◽

Akitaka Muta ◽

Kenji Ishibashi ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Brain Stem ◽

Cardiovascular Response ◽

Human Subjects ◽

Insular Cortex ◽

Brain Regions ◽

Dynamic Exercise ◽

The Brain

AbstractDynamic exercise elicits fluctuations in blood pressure (BP) and cerebral blood flow (CBF). This study investigated responses in BP and CBF during cycling exercise and post-exercise hypotension (PEH) using positron emission tomography (PET). CBF was measured using oxygen-15-labeled water (H2 15O) and PET in 11 human subjects at rest (Rest), at the onset of exercise (Ex1), later in the exercise (Ex2), and during PEH. Global CBF significantly increased by 13% at Ex1 compared with Rest, but was unchanged at Ex2 and during PEH. Compared with at Rest, regional CBF (rCBF) increased at Ex1 (20~42%) in the cerebellar vermis, sensorimotor cortex for the bilateral legs (M1Leg and S1Leg), insular cortex and brain stem, but increased at Ex2 (28~31%) only in the vermis and M1Leg and S1Leg. During PEH, rCBF decreased compared with Rest (8~13%) in the cerebellum, temporal gyrus, piriform lobe, thalamus and pons. The areas showing correlations between rCBF and mean BP during exercise and PEH were consistent with the central autonomic network, including the brain stem, cerebellum, and hypothalamus (R2=0.25–0.64). The present study suggests that higher brain regions are coordinated through reflex centers in the brain stem in order to regulate the cardiovascular response to exercise.

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Catecholamines and the relationship between cerebral blood flow and glucose use

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1986.251.4.h824 ◽

1986 ◽

Vol 251 (4) ◽

pp. H824-H833 ◽

Cited By ~ 2

Author(s):

U. I. Tuor ◽

L. Edvinsson ◽

J. McCulloch

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Moderate Hypertension ◽

Brain Regions ◽

Dopamine Infusion ◽

Arterial Blood ◽

Norepinephrine Infusion ◽

Bbb Permeability ◽

The Relationship ◽

The Brain

The effects of hypertension induced by norepinephrine and dopamine infusion on the relationship between local cerebral blood flow (CBF) and local glucose use (GU) were examined in rats with the use of quantitative autoradiographic techniques. After rats recovered from anesthesia, dopamine or norepinephrine was infused at a rate that ensured moderate hypertension [mean arterial blood pressure (MABP) approximately 150 mmHg]. During dopamine infusion (approximately 200 micrograms X kg-1 X min-1), overall CBF-to-GU ratio throughout the brain was elevated (P less than 0.0001) when compared with saline controls. In contrast, during norepinephrine infusion (approximately 10 micrograms X kg-1 X min-1), the overall CBF-to-GU relationship was not altered significantly. The differential effect of the catecholamines was a consequence of the marked increases in local CBF and moderate decreases in GU observed during dopamine infusion, whereas during norepinephrine administration CBF and GU were not significantly altered in most brain regions. Blood-brain barrier (BBB) permeability was increased during moderate hypertension induced by dopamine and not when induced by norepinephrine. During extreme hypertension (MABP greater than 165 mmHg), heterogeneous increases in CBF and BBB permeability occurred (e.g., in the cerebellum and thalamus). Thus the cerebrovascular response to catecholamine infusion was critically dependent on the agent administered, the level of hypertension achieved, and the brain region examined.

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Correlation between Cerebral Blood Flow and ATP Content following Tourniquet-Induced Ischemia in Cat Brain

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1984.53 ◽

1984 ◽

Vol 4 (3) ◽

pp. 362-367 ◽

Cited By ~ 19

Author(s):

Val Robert Marcy ◽

Frank A. Welsh

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Energy Metabolism ◽

Present Model ◽

Surgical Decompression ◽

Atp Content ◽

Atp Levels ◽

Secondary Failure ◽

Cat Brain ◽

The Brain

Cerebral ischemia was produced in anesthetized cats using a neck tourniquet, which diminished cortical blood flow to <2 ml/100 g/min and depleted levels of ATP throughout the brain. Following a 30-min insult, cortical flow measured with H2 electrodes returned nearly to control, but subsequently decreased to 14–47% of control values. Despite this secondary hypoperfusion, ATP levels adjacent to the H2 electrode were restored to 75% of normal during the 2-h recirculation period. Therefore, this degree of hypoperfusion did not cause a secondary failure of energy metabolism. Following a 60-min insult, impaired reperfusion prevented the regeneration of brain ATP. However, preischemic bilateral craniectomies significantly improved recovery of blood flow and ATP levels following 60 min of ischemia. Therefore, in the present model, insufficient reflow is a primary factor limiting recovery of energy metabolism. Further, surgical decompression prevented the occurrence of “no reflow” caused by 60 min of ischemia.

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Beta-receptor-mediated increase in cerebral blood flow during hypoglycemia

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1987.253.4.h949 ◽

1987 ◽

Vol 253 (4) ◽

pp. H949-H955 ◽

Cited By ~ 1

Author(s):

B. R. Hollinger ◽

R. M. Bryan

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Adrenergic Receptor ◽

Regional Cerebral Blood ◽

Receptor Stimulation ◽

Beta Adrenergic ◽

Beta Receptor ◽

Normoglycemic Control ◽

The Brain ◽

Oxide Anesthesia

We tested the hypothesis that beta-adrenergic receptor stimulation is involved with the increase in regional cerebral blood flow (rCBF) during hypoglycemia. Rats were surgically prepared with the use of halothane-nitrous oxide anesthesia. A plaster restraining cast was placed around the hindquarters, and anesthesia was discontinued. Hypoglycemia was produced by an intravenous injection of insulin (15 U/kg); normoglycemic control rats were given saline. Propranolol (1.5 mg/kg) was administered to some control and some hypoglycemic rats to block the beta-adrenergic receptors. Regional CBF was measured using 4-[N-methyl-14C]iodoantipyrine. Plasma glucose in the normoglycemic and hypoglycemic groups was approximately 6 and 1.4 mumol/ml, respectively. Regional CBF increased during hypoglycemia in rats that were not treated with propranolol. The increase varied from approximately 60 to 200% depending on the brain region. During hypoglycemia, propranolol abolished the increase in rCBF in the hypothalamus, cerebellum, and pyramidal tract. In other regions the increase in rCBF was only 33-65% of the increase in hypoglycemic rats that were not treated with propranolol. We conclude that beta-receptor stimulation plays a major role in the increase in rCBF during hypoglycemia.

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Distribution of regional cerebral blood flow in voluntarily diving rats.

Journal of Experimental Biology ◽

10.1242/jeb.201.4.549 ◽

1998 ◽

Vol 201 (4) ◽

pp. 549-558

Author(s):

G P Ollenberger ◽

N H West

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Regional Cerebral Blood Flow ◽

Regional Distribution ◽

Detailed Examination ◽

Brain Regions ◽

Regional Cerebral Blood ◽

Output Only ◽

Almost All ◽

The Brain

The distribution of regional cerebral blood flow (rCBF) was examined in conscious, voluntarily diving rats using the brain blood flow tracer N-[14C]isopropyl-p-iodoamphetamine and quantitative autoradiography. A detailed examination of the regional distribution of cerebral blood flow revealed that almost all brain regions were hyperperfused during diving. During diving, rCBF increased by an average of 1.7-fold in 29 of the 33 brain regions examined, despite a 69.2 % decrease in cardiac output. Only some regions of the basal ganglia (caudate-putamen and globus pallidus) and limbic areas (hippocampus and amygdala) did not increase rCBF significantly during diving. We determined that the increase in rCBF during diving is primarily due to a corresponding 20.9 % decrease in cerebrovascular resistance. A significant increase in perfusion pressure during diving also potentially contributed to the increase in rCBF. Because some brain regions did not increase flow significantly during diving, these results suggest that not all brain regions participate equally in the global cerebrovascular response to diving. This study provides evidence to support the view that the brain is preferentially perfused during conscious voluntary diving in the rat. The mechanism(s) that probably produce the cerebrovascular changes during diving are discussed.

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Vorläufige Ergebnisse von 99mTc-HMPAO-SPECT-Untersuchungen bei endogenen Psychosen

Nuklearmedizin ◽

10.1055/s-0038-1629475 ◽

1989 ◽

Vol 28 (03) ◽

pp. 88-91

Author(s):

J. Schröder ◽

H. Henningsen ◽

H. Sauer ◽

P. Georgi ◽

K.-R. Wilhelm

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Regional Cerebral Blood Flow ◽

Regions Of Interest ◽

Post Mortem ◽

Regional Cerebral Blood ◽

Hmpao Spect ◽

Endogenous Psychoses ◽

The Brain ◽

99Mtc Hmpao

18 psychopharmacologically treated patients (7 schizophrenics, 5 schizoaffectives, 6 depressives) were studied using 99mTc-HMPAO-SPECT of the brain. The regional cerebral blood flow was measured in three transversal sections (infra-/supraventricular, ventricular) within 6 regions of interest (ROI) respectively (one frontal, one parietal and one occipital in each hemisphere). Corresponding ROIs of the same section in each hemisphere were compared. In the schizophrenics there was a significantly reduced perfusion in the left frontal region of the infraventricular and ventricular section (p < 0.02) compared with the data of the depressives. The schizoaffectives took an intermediate place. Since the patients were treated with psychopharmaca, the result must be interpreted cautiously. However, our findings seem to be in accordance with post-mortem-, CT- and PET-studies presented in the literature. Our results suggest that 99mTc-HMPAO-SPECT may be helpful in finding cerebral abnormalities in endogenous psychoses.

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Neuroimaging in Drug Discovery and Development: Paradigms for Accelerating New Drug Availability

Journal of Pharmacy Practice ◽

10.1106/bx9p-gcm4-gtef-jghn ◽

2001 ◽

Vol 14 (5) ◽

pp. 407-415

Author(s):

John T. Metz ◽

Malcolm D. Cooper ◽

Terry F. Brown ◽

Leann H. Kinnunen ◽

Declan J. Cooper

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Glucose Metabolism ◽

Phase Ii ◽

New Drugs ◽

Central Effects ◽

Drug Discovery And Development ◽

Psychological Tasks ◽

The Brain ◽

Phase Iv

The process of discovering and developing new drugs is complicated. Neuroimaging methods can facilitate this process. An analysis of the conceptual bases and practical limitations of different neuroimaging modalities reveals that each technique can best address different kinds of questions. Radioligand studies are well suited to preclinical and Phase II questions when a compound is known or suspected to affect well-understood mechanisms; they are also useful in Phase IV to characterize effective agents. Cerebral blood flow studies can be extremely useful in evaluating the effects of a drug on psychological tasks (mostly in Phase IV). Glucose metabolism studies can answer the simplest questions about whether a compound affects the brain, where, and how much. Such studies are most useful in confirming central effects (preclinical and early clinical phases), in determining effective dose ranges (Phase II), and in comparing different drugs (Phase IV).

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