| Altered cellular metabolism following traumatic brain injury: a magnetic resonance spectroscopy study. | |
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MedLine Citation:
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PMID: 11284544 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Experimental studies have reported early reductions in pH, phosphocreatine, and free intracellular magnesium following traumatic brain injury using phosphorus magnetic resonance spectroscopy. Paradoxically, in clinical studies there is some evidence for an increase in the pH in the subacute stage following traumatic brain injury. We therefore performed phosphorus magnetic resonance spectroscopy on seven patients in the subacute stage (mean 9 days postinjury) following traumatic brain injury to assess cellular metabolism. In areas of normal-appearing white matter, the pH was significantly alkaline (patients 7.09 +/- 0.04 [mean +/- SD], controls 7.01 +/- 0.04, p = 0.008), the phosphocreatine to inorganic phosphate ratio (PCr/Pi) was significantly increased (patients 4.03 +/- 1.18, controls 2.64 +/- 0.71, p = 0.03), the inorganic phosphate to adenosine triphosphate ratio (Pi/ATP) was significantly reduced (patients 0.37 +/- 0.10, controls 0.56 +/- 0.19, p = 0.04), and the PCr/ATP ratio was nonsignificantly increased (patients 1.53 +/- 0.29, controls 1.34 +/- 0.19, p = 0.14) in patients compared to controls. Furthermore, the calculated free intracellular magnesium was significantly increased in the patients compared to the controls (patients 0.33 +/- 0.09 mM, controls 0.22 +/- 0.09 mM, p = 0.03)). Proton spectra, acquired from similar regions showed a significant reduction in N-acetylaspartate (patients 9.64 +/- 2.49 units, controls 12.84 +/- 2.35 units, p = 0.03) and a significant increase in choline compounds (patients 7.96 +/- 1.02, controls 6.67 +/- 1.01 units, p = 0.03). No lactate was visible in any patient or control spectrum. The alterations in metabolism observed in these patients could not be explained by ongoing ischemia but might be secondary to a loss of normal cellular homeostasis or a relative alteration in the cellular population, in particular an increase in the glial cell density, in these regions. |
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Authors:
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M R Garnett; R G Corkill; A M Blamire; B Rajagopalan; D N Manners; J D Young; P Styles; T A Cadoux-Hudson |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of neurotrauma Volume: 18 ISSN: 0897-7151 ISO Abbreviation: J. Neurotrauma Publication Date: 2001 Mar |
Date Detail:
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Created Date: 2001-04-03 Completed Date: 2001-08-09 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8811626 Medline TA: J Neurotrauma Country: United States |
Other Details:
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Languages: eng Pagination: 231-40 Citation Subset: IM |
Affiliation:
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Department of Biochemistry, University of Oxford, United Kingdom. Mg@bioch.ox.ac.uk |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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metabolism* Adolescent Adult Aspartic Acid / analogs & derivatives, metabolism Brain / metabolism*, pathology Brain Injuries / diagnosis, metabolism* Choline / metabolism Creatine / metabolism Female Humans Hydrogen-Ion Concentration Magnetic Resonance Spectroscopy / methods* Male Middle Aged Phosphates / metabolism* Phosphocreatine / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/Phosphates; 56-65-5/Adenosine Triphosphate; 56-84-8/Aspartic Acid; 57-00-1/Creatine; 62-49-7/Choline; 67-07-2/Phosphocreatine; 997-55-7/N-acetylaspartate |
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