Abstract
An electron spin resonance technique was used to measure cerebral antioxidant activity during asphyxial cardiac arrest and reperfusion. There were significant decreases in ascorbate (48%), glutathione (44%), total thiols (42%), protein thiols (38%) and alpha-tocopherol (26%) in the hippocampus 10 min after reperfusion (p < 0.05 vs respective baselines) but not during asphyxial cardiac arrest. The levels of antioxidants returned to baseline values by 120 min after reperfusion. The results support the hypothesis that reperfusion from asphyxial cardiac arrest, but not arrest alone, produced a significant oxidative stress as reflected by a depletion of both water and lipid soluble antioxidants. Furthermore, antioxidant depletion was transient, with normal antioxidant levels observed 120 min, 24 h and 72 h after reperfusion.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Antioxidants / metabolism*
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Ascorbic Acid / metabolism
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Asphyxia / metabolism
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Carbon Dioxide / blood
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Consciousness
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Cranial Nerves / physiopathology
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Electron Spin Resonance Spectroscopy / methods
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Glutathione / metabolism
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Heart Arrest / metabolism
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Hippocampus / metabolism*
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Monophenol Monooxygenase / metabolism
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Myocardial Ischemia / metabolism*
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Myocardial Ischemia / physiopathology
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Myocardial Reperfusion*
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Nerve Tissue Proteins / metabolism
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Oxidative Stress
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Oxygen / blood
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Partial Pressure
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Rats
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Rats, Sprague-Dawley
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Respiration
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Sulfhydryl Compounds / metabolism
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Time Factors
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Vitamin E / metabolism
Substances
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Antioxidants
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Nerve Tissue Proteins
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Sulfhydryl Compounds
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Vitamin E
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Carbon Dioxide
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Monophenol Monooxygenase
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Glutathione
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Ascorbic Acid
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Oxygen