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Cerebral Energy Metabolism During Severe Ischemia of Varying Duration and Following Reperfusion
Author(s) -
Phillis J. W.,
O'Regan M. H.,
Estevez A. Y.,
Song D.,
VanderHeide S. J.
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.67041525.x
Subject(s) - ischemia , adenosine , medicine , adenine nucleotide , energy metabolism , anesthesia , limiting , endocrinology , chemistry , biochemistry , nucleotide , mechanical engineering , engineering , gene
Abstract: Changes in cerebral cortical adenine nucleotide and adenosine levels during 10‐, 20‐, or 40‐min periods of four‐vessel occlusion producing cerebral ischemia in rats and reperfusions of 10, 45, or 90 min were determined to evaluate the effects of ischemia duration on mitochondrial function. Substantial recovery was evident following 10 or 20 min of cerebral ischemia but not, however, after a 40‐min period of ischemia. A secondary decline in the cortical levels of ATP became evident following 40 min of cerebral ischemia and 90 min of reperfusion. Longer periods of ischemia may be associated with a loss of adenosine, limiting the resynthesis of ATP during reperfusion. A separate group of rats, resuscitated with 100% O 2 , demonstrated a more rapid recovery of mitochondrial function compared with animals that received room air during reperfusion following 20 min of cerebral ischemia. No detrimental effects of 100% O 2 were observed during the 90‐min period of reperfusion, indicating that 100% O 2 does not promote early mitochondrial dysfunction.