TY - JOUR
T1 - Metabolite changes in neonatal rat brain during and after cerebral hypoxia-ischemia
T2 - A magnetic resonance spectroscopic imaging study
AU - Malisza, K. L.
AU - Kozlowski, P.
AU - Ning, G.
AU - Bascaramurty, S.
AU - Tuor, U. I.
PY - 1999/2
Y1 - 1999/2
N2 - Cerebral metabolite concentrations were measured in infant rats using proton magnetic resonance spectroscopic imaging. Measurements were made prior to, during and after exposure of rats (6- and 7-day-old) to unilateral cerebral hypoxia-ischemia (right carotid artery occlusion +2 h 8% oxygen). Data clustered according to age and outcome - 6-day-old animals with no infarct and 7-day-old animals with infarct. In 6-day-old animals, cerebral lactate concentration increased during hypoxia-ischemia, particularly ipsilateral to the occlusion, and returned to normal soon after the end of hypoxia. There were no major changes in N-acetyl-aspartate levels (NAA) in this group and no regions of hyperintensity on T2 or DW weighted images at 24 h. In the 7-day-old animals, lactate increased during hypoxia-ischemia and remained elevated in the first hour after reperfusion. Furthermore, lactate remained at 258 ± 117% and 233 ± 56% of pre-hypoxic levels, 24 and 48 h post-hypoxia, respectively. NAA concentrations ipsilateral to the occlusion decreased to 55 ± 14% during hypoxia, recovered early post-hypoxia and again decreased to 61 ± 25% and 41 ± 28% at 24 and 48 h post-hypoxia-ischemia, respectively. The infarct volumes measured by diffusion weighted and T2 weighted MRI at 48h post-hypoxia were 152 ± 40 mm3 and 172 ± 35 mm3, respectively. Thus, irreversible damage correlated well with measured in vivo lactate and NAA changes. Those animals in which NAA was unaltered and lactate recovered soon after hypoxia did not show long-term damage (6-day-old animals), whereas those animals in which NAA decreased and lactate remained elevated went on to infarction (7-day-old animals).
AB - Cerebral metabolite concentrations were measured in infant rats using proton magnetic resonance spectroscopic imaging. Measurements were made prior to, during and after exposure of rats (6- and 7-day-old) to unilateral cerebral hypoxia-ischemia (right carotid artery occlusion +2 h 8% oxygen). Data clustered according to age and outcome - 6-day-old animals with no infarct and 7-day-old animals with infarct. In 6-day-old animals, cerebral lactate concentration increased during hypoxia-ischemia, particularly ipsilateral to the occlusion, and returned to normal soon after the end of hypoxia. There were no major changes in N-acetyl-aspartate levels (NAA) in this group and no regions of hyperintensity on T2 or DW weighted images at 24 h. In the 7-day-old animals, lactate increased during hypoxia-ischemia and remained elevated in the first hour after reperfusion. Furthermore, lactate remained at 258 ± 117% and 233 ± 56% of pre-hypoxic levels, 24 and 48 h post-hypoxia, respectively. NAA concentrations ipsilateral to the occlusion decreased to 55 ± 14% during hypoxia, recovered early post-hypoxia and again decreased to 61 ± 25% and 41 ± 28% at 24 and 48 h post-hypoxia-ischemia, respectively. The infarct volumes measured by diffusion weighted and T2 weighted MRI at 48h post-hypoxia were 152 ± 40 mm3 and 172 ± 35 mm3, respectively. Thus, irreversible damage correlated well with measured in vivo lactate and NAA changes. Those animals in which NAA was unaltered and lactate recovered soon after hypoxia did not show long-term damage (6-day-old animals), whereas those animals in which NAA decreased and lactate remained elevated went on to infarction (7-day-old animals).
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U2 - 10.1002/(SICI)1099-1492(199902)12:1<31::AID-NBM544>3.0.CO;2-M
DO - 10.1002/(SICI)1099-1492(199902)12:1<31::AID-NBM544>3.0.CO;2-M
M3 - Article
C2 - 10195327
AN - SCOPUS:0032976349
SN - 0952-3480
VL - 12
SP - 31
EP - 38
JO - NMR in Biomedicine
JF - NMR in Biomedicine
IS - 1
ER -