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Metabolite changes in neonatal rat brain during and after cerebral hypoxia-ischemia: a magnetic resonance spectroscopic imaging study

✍ Scribed by K. L. Malisza; P. Kozlowski; G. Ning; S. Bascaramurty; U. I. Tuor


Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
131 KB
Volume
12
Category
Article
ISSN
0952-3480

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✦ Synopsis


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 T 2 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 AE 117% and 233 AE 56% of pre-hypoxic levels, 24 and 48 h post-hypoxia, respectively. NAA concentrations ipsilateral to the occlusion decreased to 55 AE 14% during hypoxia, recovered early post-hypoxia and again decreased to 61 AE 25% and 41 AE 28% at 24 and 48 h post-hypoxia-ischemia, respectively. The infarct volumes measured by diffusion weighted and T 2 weighted MRI at 48 h post-hypoxia were 152 AE 40 mm 3 and 172 AE 35 mm 3 , 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).