Delayed Onset of Neurologic Deterioration Following Anoxia Ischemia Coincides with Appearance of Impaired Brain Mitochondrial Respiration and Decreased Cytochrome Oxidase Activity

We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of o...

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Bibliographic Details
Published in:Journal of cerebral blood flow and metabolism 1990-05, Vol.10 (3), p.417-423
Main Authors: Wagner, Kenneth R., Kleinholz, Marla, Myers, Ronald E.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Brain - metabolism
Brain Ischemia - metabolism
Cats
Electron Transport Complex IV - metabolism
Hyperglycemia - metabolism
Hypoglycemia - metabolism
Hypoxia - metabolism
Medical sciences
Mitochondria - metabolism
Nervous System Diseases - metabolism
Nervous system involvement in other diseases. Miscellaneous
Neurology
Oxygen Consumption
Respiratory Transport
Space life sciences
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Summary:We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of onset of mitochondrial dysfunction and neurologic signs was unclear, in the present study we killed postanoxic cats immediately when signs first appeared. Cerebrocortical homogenates and isolated brain mitochondria only from symptomatic cats showed markedly inhibited substrate-, ADP-, and uncoupler-stimulated respiration rates. Cytochrome oxidase activity and cytochrome aa3 concentrations were also markedly reduced in these mitochondria. Since brain mitochondrial function was impaired when neurologic signs first appeared, mitochondrial alterations are an important early organellar change correlated with development of neurologic deterioration following anoxia.
ISSN:0271-678X
1559-7016
DOI:10.1038/jcbfm.1990.72