Abstract
Derangements in the concentrations of the adenine nucleotides are a common occurrence during and after an ischemic episode. ATP levels decrease rapidly at the onset of ischemia and remain depressed for the entire period of ischemia (12, 24). Upon recirculation of the tissue, the extent of ATP restoration depends on the duration of the ischemic insult. For example, the ATP levels were completely regenerated at 60 min of recirculation following 1 and 5 min of bilateral occlusion, but not after 20 and 60 min (16). The total adenylates (sum of ATP + ADP + AMP) decrease somewhat more slowly during ischemia; in decapitated mouse forebrains, the half-time for the disappearance of total adenylates was approximately 32 min. The total adenylates were also very slow to recover. Ljunggren et al. (10) reported that the levels were significantly less than control at 3 hours after a 3 min ischemic interval. Since the hydrolysis of ATP is the major source of energy for a host of biochemical processes, alterations in adenine nucleotide metabolism resulting from ischemia could have pronounced effects on brain function and therefore on the likelihood of survival after ischemia.
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© 1980 Plenum Press, New York
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Murakami, N., Lust, W.D., de Azeredo, F.A.M., Passonneau, J.V. (1980). Ischemia Related Changes in Adenine Nucleotide Metabolism. In: Spatz, M., Mršulja, B.B., Rakić, L.M., Lust, W.D. (eds) Circulatory and Developmental Aspects of Brain Metabolism. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3836-9_2
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