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Departments of 1 Surgery and 2 Medicine, University of Louisville School of Medicine, Louisville, Kentucky 40292
Hepatic hypothermia can safely
prolong the duration of hepatic inflow occlusion during complex liver
resectional surgeries. The mechanism(s) by which hypothermia protects
against this form of liver ischemia-reperfusion injury are not
completely understood. In this study, we sought to determine whether
hypothermia protects against ischemia-reperfusion injury by altering
the hepatic inflammatory response. Mice undergoing 90 min of partial
hepatic ischemia followed by up to 8 h of reperfusion had their
body temperatures regulated at 35-37°C (normothermic) or
unregulated, in which rectal temperature dropped as low as 25°C by
the end of ischemia (hypothermic). Hypothermic mice had less liver
injury vs. normothermic mice, as assessed histologically, by serum
transaminase levels (89% decrease), and by liver wet-to-dry weight
ratios (91% decrease). Neutrophil accumulation was absent in
hypothermic mice (99% reduction vs. normothermic mice). Production of
the proinflammatory cytokines tumor necrosis factor-
,
interleukin-1
, and macrophage inflammatory protein-2 were reduced by
up to 92%. Activation of the transcription factor nuclear factor-
B
was not reduced in hypothermic mice, but activation of c-Jun
NH2-terminal kinase (JNK) and the transcription factor activator protein (AP)-1 were greatly diminished. These data suggest that hypothermia suppresses the hepatic inflammatory response through
selective inhibition of JNK and AP-1.
inflammation; cytokines; neutrophils
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