title: Impact of intraischemic temperature on oxidative stress during hepatic reperfusion.
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.
authors.affiliation: Institute for Surgical Research, University of Munich, Munich, Germany. andrej.khandoga@icf.med.uni-muenchen.de
authors.forename: Andrej
authors.initials: A
authors.lastname: Khandoga
authors.forename: Georg
authors.initials: G
authors.lastname: Enders
authors.forename: Benjamin
authors.initials: B
authors.lastname: Luchting
authors.forename: Stefan
authors.initials: S
authors.lastname: Axmann
authors.forename: Thomas
authors.initials: T
authors.lastname: Minor
authors.forename: Ulf
authors.initials: U
authors.lastname: Nilsson
authors.forename: Peter
authors.initials: P
authors.lastname: Biberthaler
authors.forename: Fritz
authors.initials: F
authors.lastname: Krombach
mesh_terms: D000249:Adenosine Monophosphate / Q000378:metabolism; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D004195:Disease Models, Animal; D004578:Electron Spin Resonance Spectroscopy; D005260:Female; D006419:Heme Oxygenase (Decyclizing) / Q000235:genetics; D051547:Heme Oxygenase-1; D017665:Hydroxyl Radical; D007036:Hypothermia, Induced; D015227:Lipid Peroxidation; D008099:Liver / Q000098:blood supply*; D008565:Membrane Proteins; D051379:Mice; D008810:Mice, Inbred C57BL; D008833:Microcirculation; D018384:Oxidative Stress; D012333:RNA, Messenger / Q000378:metabolism; D015424:Reperfusion; D015427:Reperfusion Injury / Q000503:physiopathology*; D013482:Superoxide Dismutase / Q000235:genetics; D000072105:Superoxide Dismutase-1; D013696:Temperature
chemical_list: D008565:Membrane Proteins; D012333:RNA, Messenger; D017665:Hydroxyl Radical; D000249:Adenosine Monophosphate; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; C496542:Hmox1 protein, mouse; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D001205:Ascorbic Acid