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Mitochondrial dysfunction following cardiac arrest and resuscitation in rat brain
Author(s) -
Xu Kui,
Puchowicz Michelle A,
Sun Xiaoyan,
LaManna Joseph C
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a227-b
Subject(s) - resuscitation , mitochondrion , medicine , anesthesia , oxidative stress , hippocampus , oxidative phosphorylation , endocrinology , biology , biochemistry
Cardiac arrest and resuscitation results in reperfusion injury associated with oxidative stress, leading to delayed selective neuronal cell loss and post‐resuscitation mortality in rats. The mitochondrial respiratory chain has been recognized as the major source and target of free radicals during reperfusion. In this study we investigated the mitochondrial function of rat brain following cardiac arrest and resuscitation. Male Wistar rats (3‐month) were subjected to cardiac arrest (~12 minutes) and allowed to recover up to 2 days after resuscitation. Mitochondria of cortex, brainstem and hippocampus were freshly isolated and ADP‐stimulated oxidative rates (state 3, ADP‐stimulated and state 4, ADP‐limited) were assessed by measuring oxygen consumption (polarographically) in the presence of substrates (glutamate + malate). Compared to the non‐arrested control group, the respiratory control ratios (RCR) at 1 hr and 1 day recovery were about 30% lower in all regions. State 3 rates were slightly higher, but state 4 rates were increased by half. The RCR returned to baseline at 2 days. The higher state 4 rates suggest that mitochondria during the first day after reperfusion were partially uncoupled.