Effects of Traumatic Brain Injury on Cerebral High-Energy Phosphates and pH: A31P Magnetic Resonance Spectroscopy Study

Abstract

Traumatic injuries to the CNS produce tissue damage both through mechanical disruption and through more delayed autodestructive processes. Delayed events include various biochemical changes whose nature and time course remain to be fully elucidated. Magnetic resonance spectroscopy (MRS) techniques permit repeated, noninvasive measurement of biochemical changes in the same animal. Using phosphorus MRS, we have examined certain biochemical responses of rats over an 8-h period following lateralized brain injury (1.5–2.5 atmospheres) using a standardized fluid-percussion model recently developed in our laboratory. Following injury, the ratio of phosphocreatine to inorganic phosphate (PCr/Pi) showed a biphasic decline: The first decline reached its nadir (4.8 ± 0.4 to 2.8 ± 0.7) by 40 min post-trauma with recovery by 100 min, followed by a second decline by 2 h that persisted for the remaining 6-h observation period (mean 2.5 ± 0.5). The first, but not the second, decrease in PCr/Piwas associated with tissue acidosis (pH 7.10 ± 0.03 to 6.86 ± 0.11). No changes in ATP occurred at any time during the injury observation period. Such changes may be indicative of altered mitochondrial energy production following brain injury, which may account for the reduced capacity of the cell to recover from traumatic injury.