Metabolic imaging of energy metabolism in traumatic brain injury using hyperpolarized [1-13C]pyruvate

• Published in: Scientific reports Vol. 7; no. 1; pp. 1907 - 7
• Main Authors: DeVience, Stephen J., Lu, Xin, Proctor, Julie, Rangghran, Parisa, Melhem, Elias R., Gullapalli, Rao, Fiskum, Gary M., Mayer, Dirk
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 15.05.2017; Nature Publishing Group; Nature Portfolio
• Subjects: 140/131; 59; 59/57; 631/1647/245/1628; 692/53/2421; 692/617/375/1345; Aerobic respiration; Animals; Bicarbonates; Brain Injuries, Traumatic - diagnostic imaging; Brain Injuries, Traumatic - metabolism; Brain Injuries, Traumatic - pathology; Carbon Isotopes; Cortex; Disease Models, Animal; Electron transport; Energy Metabolism; Humanities and Social Sciences; Image Processing, Computer-Assisted; Lactic acid; Magnetic resonance imaging; Magnetic Resonance Imaging - methods; Magnetic resonance spectroscopy; Male; Metabolism; Mitochondria; Molecular Imaging - methods; multidisciplinary; Neuroimaging; Pyruvic acid; Pyruvic Acid - metabolism; Rats; Science; Science (multidisciplinary); Traumatic brain injury
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-017-01736-x

Traumatic brain injury (TBI) is known to cause perturbations in the energy metabolism of the brain, but current tests of metabolic activity are only indirect markers of energy use or are highly invasive. Here we show that hyperpolarized 13 C magnetic resonance spectroscopic imaging (MRSI) can be used as a direct, non-invasive method for studying the effects of TBI on energy metabolism. Measurements were performed on rats with moderate TBI induced by controlled cortical impact on one cerebral hemisphere. Following injection of hyperpolarized [1- 13 C]pyruvate, the resulting 13 C-bicarbonate signal was found to be 24 ± 6% lower in the injured hemisphere compared with the non-injured hemisphere, while the hyperpolarized bicarbonate-to-lactate ratio was 33 ± 8% lower in the injured hemisphere. In a control group, no significant difference in signal was found between sides of the brain. The results suggest an impairment in mitochondrial pyruvate metabolism, resulting in a decrease in aerobic respiration at the location of injury following TBI.