Impact of intraischemic temperature on oxidative stress during hepatic reperfusion

This study was designed to investigate the influence of intraischemic liver temperature on oxidative stress during postischemic normothermic reperfusion. In C57BL/6 mice, partial hepatic ischemia was induced for 90 min and intraischemic organ temperature adjusted to 4°C, 15°C, 26°C, 32°C, and 37°C....

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Published in:Free radical biology & medicine 2003-10, Vol.35 (8), p.901-909
Main Authors: Khandoga, Andrej, Enders, Georg, Luchting, Benjamin, Axmann, Stefan, Minor, Thomas, Nilsson, Ulf, Biberthaler, Peter, Krombach, Fritz
Format: Article
Language:English
Subjects:
Adenosine Monophosphate - metabolism
Animals
Ascorbic Acid - metabolism
Disease Models, Animal
Electron Spin Resonance Spectroscopy
Female
Free radicals
Heme Oxygenase (Decyclizing) - genetics
Heme Oxygenase-1
Hydroxyl Radical
Hypothermia, Induced
Ischemia
Ischemic temperature
Lipid Peroxidation
Liver
Liver - blood supply
Membrane Proteins
Mice
Mice, Inbred C57BL
Microcirculation
Oxidative Stress
Reactive oxygen species
Reperfusion
Reperfusion Injury - physiopathology
RNA, Messenger - metabolism
Superoxide Dismutase - genetics
Superoxide Dismutase-1
Temperature
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Summary:This study was designed to investigate the influence of intraischemic liver temperature on oxidative stress during postischemic normothermic reperfusion. In C57BL/6 mice, partial hepatic ischemia was induced for 90 min and intraischemic organ temperature adjusted to 4°C, 15°C, 26°C, 32°C, and 37°C. As detected by electron spin-resonance spectroscopy, plasma/blood concentrations of hydroxyl and ascorbyl radicals were significantly increased in all groups after ischemia/reperfusion independent of the intraischemic temperature. In tissue, however, postischemic lipid peroxidation was attenuated after organ cooling down to 32°C–26°C and not detectable after ischemia at 15°C–4°C. mRNA expression of superoxide dismutase-1 and heme oxygenase-1, measured during reperfusion, was significantly elevated in the group at 37°C as compared to the hypothermic groups at 4°C–32°C. The reduction of radical generation was associated with a prevention of adenosine monophosphate hydrolysis during ischemia in the hypothermic groups. In conclusion, ischemia-reperfusion-induced oxidative stress in the liver tissue is non-linearly-dependent on intraischemic temperature, whereas the plasma/blood concentration of radicals is not affected by organ cooling. Oxidative stress is reduced through mild hypothermia at 32°C–26°C and inhibited completely at 15°C. Reduction of initial intracellular radical generation and prevention of secondary oxidant-induced tissue injury are possible mechanisms of this protection.
ISSN:0891-5849
1873-4596
DOI:10.1016/S0891-5849(03)00430-1