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).
|Original language||English (US)|
|Number of pages||8|
|Journal||NMR in Biomedicine|
|State||Published - Feb 1999|
All Science Journal Classification (ASJC) codes
- Molecular Medicine
- Radiology Nuclear Medicine and imaging