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Metabolites
Special Issues
Cerebral Metabolism
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Cerebral Metabolism

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (31 December 2020) | Viewed by 5121

Special Issue Editors

Prof. Dr. Frantz Rom Poulsen

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Guest Editor
Department of Neurosurgery, Odense University Hospital, University of Southern Denmark, Sdr. Boulevard 29, 5000 Odense C, Denmark
Interests: cerebral metabolism; high grade glioma surgery; meningioma surgery; chronic subdural hematoma; hydrocephalus
Dr. Troels Halfeld Nielsen

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Guest Editor
Department of Neurosurgery, Odense University Hospital, University of Southern Denmark, Sdr. Boulevard 29, 5000 Odense C, Denmark
Interests: cerebral metabolism; cerebral aneurysms; cerebral vascular malformations
Dr. Axel Forsse

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Guest Editor
Department of Neurosurgery, Odense University Hospital, University of Southern Denmark, Sdr. Boulevard 29, 5000 Odense C, Denmark
Interests: cerebral metabolism; microdialysis; stroke neuroprotection; multimodal monitoring; subarachnoid hemorrhage

Special Issue Information

Dear Colleagues,

Cerebral metabolism plays a vital role in several severe brain disorders, including subarachnoidal hemorrhage, cerebral ischemia, intracranial hemorrhages, severe head trauma, severe bacterial meningitis, etc. There are ample data from animal experiments as well as observational data from clinical studies suggesting that dysfunctions in cerebral metabolism can potentially accentuate the damage initiated by the primary brain lesion. Such secondary damage could be preventable by detailed knowledge of the underlying basic mechanisms and counteracting tailored therapies.

Monitoring cerebral metabolism in clinical settings is being used more and more. This development is aided by the technological achievements.

This Special Issue will focus on all aspects of cerebral metabolism studies, both clinical and preclinical. We invite research articles, reviews and short communications for submission. Specific areas include but are not limited to multimodal monitoring and its use in monitoring cerebral metabolism to predict disease progression and outcome. In addition, we also invite manuscripts with innovative and integrative solutions that can potentially aid clinicians in optimizing the cerebral metabolism of the individual patients, thereby improving patient outcome.

Prof. Dr. Frantz Rom Poulsen
Dr. Troels Halfeld Nielsen
Dr. Axel Forsse
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Cerebral metabolism
  • Microdialysis
  • Mitochondrial dysfunction
  • Multimodal monitoring

Published Papers (2 papers)

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12 pages, 3087 KiB  
Article
Ethyl Pyruvate Increases Post-Ischemic Levels of Mitochondrial Energy Metabolites: A 13C-Labeled Cerebral Microdialysis Study
by Kevin H. Nygaard, Jesper F. Havelund, Troels H. Nielsen, Carl-Henrik Nordström, Nils. J. Færgeman, Frantz R. Poulsen, Jan Bert Gramsbergen and Axel Forsse
Metabolites 2020, 10(7), 287; https://doi.org/10.3390/metabo10070287 - 13 Jul 2020
Cited by 5 | Viewed by 2803
Abstract
Mitochondrial dysfunction after transient cerebral ischemia can be monitored by cerebral microdialysis (CMD) using changes in the lactate and pyruvate concentrations and ratio. Other metabolites associated with mitochondrial (dys)function are, e.g., tricyclic acid (TCA) and purine metabolites. Ethyl pyruvate (EP) is a putative [...] Read more.
Mitochondrial dysfunction after transient cerebral ischemia can be monitored by cerebral microdialysis (CMD) using changes in the lactate and pyruvate concentrations and ratio. Other metabolites associated with mitochondrial (dys)function are, e.g., tricyclic acid (TCA) and purine metabolites. Ethyl pyruvate (EP) is a putative neuroprotectant, supposedly targeting mitochondrial energy metabolism, but its effect on cerebral energy metabolism has never been described using microdialysis. In this study we monitored the metabolic effects of EP in the endothelin-1 (ET-1) rat model using perfusion with 13C-succinate and analysis of endogenous and 13C-labeled metabolites in the dialysates by liquid chromatography-mass spectrometry (LC-MS). Adult Sprague Dawley rats (n = 27 of which n = 11 were included in the study) were subjected to the microdialysis experiments. Microdialysis probes were perfused with 13C-labeled succinate (1 mM), and striatal dialysates were collected at 30 min intervals before induction of the insult, during intracerebral application of ET-1, and during intravenous treatment with either EP (40 mg/kg) or placebo, which was administered immediately after the insult. The rats were subjected to transient cerebral ischemia by unilateral microinjection of ET-1 in the piriform cortex, causing vasoconstriction of the medial cerebral artery. Monitoring was continued for 5 h after reperfusion, and levels of endogenous and 13C-labeled energy metabolites before and after ischemia-reperfusion were compared in EP-treated and control groups. Infarct volumes were assessed after 24 h. In both the EP-treated and placebo groups, ET-1-induced vasoconstriction resulted in a transient depression of interstitial glucose and elevation of lactate in the ipsilateral striatum. In the reperfusion phase, the concentrations of labeled malate, isocitrate, and lactate as well as endogenous xanthine were significantly higher in the EP-group than in the placebo-group: (mean ± SEM) labeled malate: 39.5% ± 14.9, p = 0.008; labeled isocitrate: 134.8% ± 67.9, p = 0.047; labeled lactate: 61% ± 22.0, p = 0.007; and endogenous xanthine: 93.9% ± 28.3, p = 0.0009. In the placebo group, significantly elevated levels of uridine were observed (mean ± SEM) 32.5% ± 12.7, p = 0.01. Infarct volumes were not significantly different between EP-treated and placebo groups, p = 0.4679. CMD labeled with 13C-succinate enabled detection of ischemic induction and EP treatment effects in the ET-1 rat model of transient focal cerebral ischemia. EP administered as a single intravenous bolus in the reperfusion-phase after transient cerebral ischemia increased de novo synthesis of several key intermediate energy metabolites (13C-malate, 13C-isocitrate, and endogenous xanthine). In summary, mitochondria process 13C-succinate more effectively after EP treatment. Full article
(This article belongs to the Special Issue Cerebral Metabolism)
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5 pages, 9340 KiB  
Case Report
Cerebral Microdialysis in Aneurismal Subarachnoid Hemorrhage Patient Reveals a Detrimental Shift in Brain Energy Metabolism, Despite Normal Perfusion Pressure
by Frederik Nielsen, Pernille Haure, Jacob Madsen, Birgitte Steenfeldt Nielsen and Carsten Reides Bjarkam
Metabolites 2020, 10(9), 341; https://doi.org/10.3390/metabo10090341 - 24 Aug 2020
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Abstract
The present case study concerns a patient admitted to our neuro-intensive care unit with a severe aneurismal subarachnoid hemorrhage rebleeding. The patient was equipped with multimodal neuromonitoring, including cerebral microdialysis. During the neuro-intensive care unit, there was a gradual decrease in cerebral perfusion [...] Read more.
The present case study concerns a patient admitted to our neuro-intensive care unit with a severe aneurismal subarachnoid hemorrhage rebleeding. The patient was equipped with multimodal neuromonitoring, including cerebral microdialysis. During the neuro-intensive care unit, there was a gradual decrease in cerebral perfusion pressure, which was within normally accepted levels, correlated to a detrimental shift in cerebral metabolism, from mitochondrial dysfunction to an ischemic pattern. Subsequently, the clinical and paraclinical status of the patient worsened. The present case highlights how the dynamic assessment of cerebral metabolic patterns and the concept of mitochondrial dysfunction can be relevant in the day-to-day clinical setting, to evaluate and optimize basic, well-known physiological parameters, such as cerebral perfusion pressure. Full article
(This article belongs to the Special Issue Cerebral Metabolism)
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