N-acetylaspartate (NAA) is a plausible marker of neuronal viability which decreases in a variety of neurodestructive conditions. To elucidate the mechanism that leads to NAA decline in two different types of cerebral ischemia in rats, we simultaneously determined cortical concentrations of NAA and its hydrolytic metabolites, aspartate, and acetate by high-resolution 1H-NMR spectroscopy. NAA decreased almost linearly up to 24 h in both decapitation induced global cerebral ischemia, and in ischemic cortices of focal ischemia. Acetate was increased continuously for up to 24 h of global ischemia, while in focal cerebral ischemia it was increased transiently at 6 h. Aspartate did not show any change in global ischemia, while it was decreased in focal ischemia. Although NAA decreased similarly in the brain with global and focal ischemia, temporal changes of two NAA hydrolytic metabolites were different in each type of ischemia. The present results suggest hydrolytic degradation of NAA may be modified alternatively under each pathophysiologic condition.