Impact of intraischemic temperature on oxidative stress during hepatic reperfusion

• 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
• ISSN: 0891-5849; 1873-4596
• DOI: 10.1016/S0891-5849(03)00430-1

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.