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N-tert-Butyl-α-Phenylnitrone Improves Recovery of Brain Energy State in Rats Following Transient Focal Ischemia

Jaroslava Folbergrova, Qi Zhao, Ken-Ichiro Katsura and Bo K. Siesjo
Proceedings of the National Academy of Sciences of the United States of America
Vol. 92, No. 11 (May 23, 1995), pp. 5057-5061
Stable URL: http://www.jstor.org/stable/2367670
Page Count: 5
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
N-tert-Butyl-α-Phenylnitrone Improves Recovery of Brain Energy State in Rats Following Transient Focal Ischemia
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Abstract

Recent results have demonstrated that the spin trapping agent N-tert-butyl-α-phenylnitrone (PBN) reduces infarct size due to middle cerebral artery occlusion (MCAO), even when given after ischemia. The objective of the present study was to explore whether PBN influences recovery of energy metabolism. MCAO of 2-hr duration was induced in rats by an intraluminal filament technique. Brains were frozen in situ at the end of ischemia and after 1, 2, and 4 hr of recirculation. PBN was given 1 hr after recirculation. Neocortical focal and perifocal ("penumbra") areas were sampled for analyses of phosphocreatine (PCr), creatine, ATP, ADP, AMP, glycogen, glucose, and lactate. The penumbra showed a moderate-to-marked decrease and the focus showed a marked decrease in PCr and ATP concentrations, a decline in the sum of adenine nucleotides, near-depletion of glycogen, and an increase in lactate concentration after 2 hr of ischemia. Recirculation for 1 hr led to only a partial recovery of energy state, with little further improvement after 2 hr and signs of secondary deterioration after 4 hr, particularly in the focus. After 4 hr of recirculation, PBN-treated animals showed pronounced recovery of energy state, with ATP and lactate contents in both focus and penumbra approaching normal values. Although an effect of PBN on mitochondria cannot be excluded, the results suggest that PBN acts by preventing a gradual compromise of microcirculation. The results justify a reevaluation of current views on the pathophysiology of focal ischemic damage and suggest that a therapeutic window of many hours exists in stroke.

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