Impact of intraischemic temperature on oxidative stress during hepatic reperfusion |
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Authors: | Khandoga Andrej Enders Georg Luchting Benjamin Axmann Stefan Minor Thomas Nilsson Ulf Biberthaler Peter Krombach Fritz |
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Affiliation: | Institute for Surgical Research, University of Munich, Munich, Germany. andrej.khandoga@icf.med.uni-muenchen.de |
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Abstract: | 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 degrees C, 15 degrees C, 26 degrees C, 32 degrees C, and 37 degrees 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 degrees C-26 degrees C and not detectable after ischemia at 15 degrees C-4 degrees C. mRNA expression of superoxide dismutase-1 and heme oxygenase-1, measured during reperfusion, was significantly elevated in the group at 37 degrees C as compared to the hypothermic groups at 4 degrees C-32 degrees 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 degrees C-26 degrees C and inhibited completely at 15 degrees C. Reduction of initial intracellular radical generation and prevention of secondary oxidant-induced tissue injury are possible mechanisms of this protection. |
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