Literature DB >> 3249310

Changes in cellular bioenergetic state following graded traumatic brain injury in rats: determination by phosphorus 31 magnetic resonance spectroscopy.

R Vink1, A I Faden, T K McIntosh.   

Abstract

Phosphorus 31 magnetic resonance spectroscopy (31P MRS) was used to study noninvasively the intracellular free Mg2+ concentration and cellular bioenergetic state of rat brain in vivo before and after fluid percussion-induced traumatic brain injury of graded severity. Brain injury was induced at four levels: low (1.0 +/- 0.5 atm); moderate (2.1 +/- 0.4 atm); high (3.9 +/- 0.9 atm); and severe (5.9 +/- 0.7 atm). Prior to injury, mean intracellular values for all groups (n = 24; mean +/- SE) were as follows: pH = 7.11 +/- 0.03; free [Mg2+] = 0.99 +/- 0.07 mM; cytosolic [ADP] = 25.2 +/- 0.8 nmol/g wet weight; cytosolic [AMP] = 0.29 +/- 0.02 nmol/g wet weight; cytosolic phosphorylation potential = 118.5 +/- 3.1 X 10(3) M-1; free energy of ATP hydrolysis = 62.11 +/- 0.04 kJ/mole; and energy charge = 0.99 +/- 0.01. Following every level of injury, there were decreases in intracellular free Mg2+ concentration, and alterations in the intracellular pH. These posttraumatic changes in Mg2+ and pH induced shifts in the equilibrium constants of the creatine kinase, adenylate kinase, and ATPase reactions, resulting in alterations in [ADP], [AMP], cytosolic phosphorylation potential, and free energy of hydrolysis, but not in the energy charge. The alterations in cytosolic phosphorylation potential following trauma were linearly correlated with the changes in intracellular free Mg2+ concentration. None of the individual bioenergetic parameters could be correlated with the severity of injury over the entire injury range; however, an association between cytosolic phosphorylation potential and reversibility of injury was apparent. These results suggest that reductions in cellular bioenergetic state following traumatic brain injury occur through a posttraumatic decrease in the cells' capacity for oxidative phosphorylation, which itself may be directly related to the intracellular free Mg2+ concentration.

Entities:  

Mesh:

Substances:

Year:  1988        PMID: 3249310     DOI: 10.1089/neu.1988.5.315

Source DB:  PubMed          Journal:  J Neurotrauma        ISSN: 0897-7151            Impact factor:   5.269


  18 in total

1.  Metabolic crisis without brain ischemia is common after traumatic brain injury: a combined microdialysis and positron emission tomography study.

Authors:  Paul Vespa; Marvin Bergsneider; Nayoa Hattori; Hsiao-Ming Wu; Sung-Cheng Huang; Neil A Martin; Thomas C Glenn; David L McArthur; David A Hovda
Journal:  J Cereb Blood Flow Metab       Date:  2005-06       Impact factor: 6.200

Review 2.  Regional brain monitoring in the neurocritical care unit.

Authors:  Jennifer Frontera; Wendy Ziai; Kristine O'Phelan; Peter D Leroux; Peter J Kirkpatrick; Michael N Diringer; Jose I Suarez
Journal:  Neurocrit Care       Date:  2015-06       Impact factor: 3.210

3.  Cerebral Energy Status and Altered Metabolism in Early Severe TBI: First Results of a Prospective 31P-MRS Feasibility Study.

Authors:  Daniel Pinggera; Ruth Steiger; Marlies Bauer; Johannes Kerschbaumer; Markus Luger; Ronny Beer; Andreas Rietzler; Astrid E Grams; Elke R Gizewski; Claudius Thomé; Ondra Petr
Journal:  Neurocrit Care       Date:  2021-04       Impact factor: 3.210

4.  Exogenous BDNF Increases Mitochondrial pCREB and Alleviates Neuronal Metabolic Defects Following Mechanical Injury in a MPTP-Dependent Way.

Authors:  Zhen Xu; Xiao-Ai Lv; Qun Dai; Man Lu; Zhang Jin
Journal:  Mol Neurobiol       Date:  2017-05-15       Impact factor: 5.590

5.  Erosion of inhibition contributes to the progression of low magnesium bursts in rat hippocampal slices.

Authors:  M A Whittington; R D Traub; J G Jefferys
Journal:  J Physiol       Date:  1995-08-01       Impact factor: 5.182

Review 6.  Cerebral blood flow and autoregulation after pediatric traumatic brain injury.

Authors:  Yuthana Udomphorn; William M Armstead; Monica S Vavilala
Journal:  Pediatr Neurol       Date:  2008-04       Impact factor: 3.372

7.  Perturbation of cellular energy state in complete ischemia: relationship to dissipative ion fluxes.

Authors:  A Ekholm; B Asplund; B K Siesjö
Journal:  Exp Brain Res       Date:  1992       Impact factor: 1.972

8.  Late exercise reduces neuroinflammation and cognitive dysfunction after traumatic brain injury.

Authors:  Chun-Shu Piao; Bogdan A Stoica; Junfang Wu; Boris Sabirzhanov; Zaorui Zhao; Rainier Cabatbat; David J Loane; Alan I Faden
Journal:  Neurobiol Dis       Date:  2013-01-08       Impact factor: 5.996

9.  The Neurometabolic Cascade of Concussion.

Authors:  Christopher C. Giza; David A. Hovda
Journal:  J Athl Train       Date:  2001-09       Impact factor: 2.860

10.  Delayed changes in regional brain energy metabolism following cerebral concussion in rats.

Authors:  Marek Buczek; Jamie Alvarez; Jaffar Azhar; Yinong Zhou; W David Lust; Warren R Selman; Robert A Ratcheson
Journal:  Metab Brain Dis       Date:  2002-09       Impact factor: 3.584

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.