TY - JOUR
T1 - High-resolution 1H NMR spectroscopy following experimental brain trauma
AU - Rubin, Yoram
AU - Cecil, Kim
AU - Wehrli, Suzanne
AU - McIntosh, Tracy K.
AU - Lenkinski, Robert E.
AU - Smith, Douglas H.
PY - 1997/7
Y1 - 1997/7
N2 - We investigated acute metabolic changes following parasagittal fluid- percussion brain injury in the rat, using high-resolution 1H nuclear magnetic resonance (NMR) spectroscopy. Sixty minutes following brain injury or sham (surgery, no injury) treatment, brains were rapidly removed and the injured and control cortices were isolated (n = 5/group). Isolates of brain cortices were then placed in buffer and studied in a 400-MHz spectrometer with measurements taken every 15 min over a 145-min period. At the initial NMR evaluation (immediately following dissection), we observed significantly lower levels of N-acetyl aspartic acid (NAA) in the injured group compared to the sham group. Surprisingly, a reciprocal increase in the concentration of acetate, a major metabolic product of NAA, was not observed at this timepoint. At subsequent timepoints, a progressive loss of NAA was observed in both injured and sham cortices, presumably due to ischemic conditions of the ex vivo samples. However, this progressive loss of NAA was now accompanied by a commensurate accumulation of acetate. These results suggest that (1) a decrease in the concentration of NAA occurs by 1 h following experimental brain trauma, potentially marking traumatic neural injury; (2) the initial absence of an expected reciprocal increase in acetate concentration may signify rapid utilization of acetate following trauma, potentially for reparative processes; and (3) in contrast to trauma alone, post morterm ischemic conditions may induce an increase in acetate concentrations.
AB - We investigated acute metabolic changes following parasagittal fluid- percussion brain injury in the rat, using high-resolution 1H nuclear magnetic resonance (NMR) spectroscopy. Sixty minutes following brain injury or sham (surgery, no injury) treatment, brains were rapidly removed and the injured and control cortices were isolated (n = 5/group). Isolates of brain cortices were then placed in buffer and studied in a 400-MHz spectrometer with measurements taken every 15 min over a 145-min period. At the initial NMR evaluation (immediately following dissection), we observed significantly lower levels of N-acetyl aspartic acid (NAA) in the injured group compared to the sham group. Surprisingly, a reciprocal increase in the concentration of acetate, a major metabolic product of NAA, was not observed at this timepoint. At subsequent timepoints, a progressive loss of NAA was observed in both injured and sham cortices, presumably due to ischemic conditions of the ex vivo samples. However, this progressive loss of NAA was now accompanied by a commensurate accumulation of acetate. These results suggest that (1) a decrease in the concentration of NAA occurs by 1 h following experimental brain trauma, potentially marking traumatic neural injury; (2) the initial absence of an expected reciprocal increase in acetate concentration may signify rapid utilization of acetate following trauma, potentially for reparative processes; and (3) in contrast to trauma alone, post morterm ischemic conditions may induce an increase in acetate concentrations.
KW - Acetate
KW - Brain injury
KW - Fluid percussion
KW - N-acetyl aspartate
KW - Nuclear magnetic resonance
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U2 - 10.1089/neu.1997.14.441
DO - 10.1089/neu.1997.14.441
M3 - Article
C2 - 9257662
AN - SCOPUS:0030610052
SN - 0897-7151
VL - 14
SP - 441
EP - 449
JO - Journal of neurotrauma
JF - Journal of neurotrauma
IS - 7
ER -