• Corpus ID: 18957736

Binge drinking disturbs hepatic microcirculation after transplantation: prevention with free radical scavengers.

@article{Zhong1999BingeDD,
  title={Binge drinking disturbs hepatic microcirculation after transplantation: prevention with free radical scavengers.},
  author={Zhi Zhong and Gavin E. Arteel and Henry D. Connor and Peter Schemmer and Shu-chuan Chou and James A. Raleigh and Ronald P. Mason and John J. Lemasters and Ronald G. Thurman},
  journal={The Journal of pharmacology and experimental therapeutics},
  year={1999},
  volume={290 2},
  pages={
          611-20
        }
}
Disturbances in hepatic microcirculation increase graft injury and failure; therefore, this study evaluates the effects of ethanol on microcirculation after liver transplantation. Donor rats were given one dose of ethanol (5 g/kg) by gavage 20 h before explantation, and grafts were stored in University of Wisconsin solution for 24 h before implantation. Acute ethanol treatment decreased 7-day survival of grafts from about 90 to 30%, increased transaminase release nearly 4-fold, and decreased… 

Figures from this paper

Role of free radicals in failure of fatty liver grafts caused by ethanol.
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Increased ICAM-1 expression in ethanol-treated fatty livers predisposes to leukocyte adherence after LT, which leads to a disturbed microcirculation, oxidative stress and graft injury.
Ischemia-reperfusion Injury after Canine Liver Allo-transplantation: The Effect of Gadolinium Chloride.
TLDR
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Repeated whiskey binges promote liver injury in rats fed a choline-deficient diet.
Intrahepatic microcirculatory disorder, parenchymal hypoxia and NOX4 upregulation result in zonal differences in hepatocyte apoptosis following lipopolysaccharide- and D-galactosamine-induced acute liver failure in rats
TLDR
The results revealed that the apoptotic cells in zone 3 were a result of hypoxic conditions induced by intrahepatic microcirculatory disorder, and were not induced by activated macrophages, and may contribute to the progression of hepatocyte apoptosis.
Binge ethanol exposure increases liver injury in obese rats.
TLDR
The data indicate that binge drinking increases apoptosis and liver injury in obese rats more than in lean controls and suggest that the injury may involve oxidative and nitrosative damage.
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References

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TLDR
Data indicate that survival is poorer and graft injury is greater in fatty livers from ethanol-treated rats and gadolinium chloride minimized graft damage, most likely by improving hepatic microcirculation and diminishing lipid peroxidation.
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TLDR
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TLDR
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TLDR
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TLDR
The hypothesis that activation of Kupffer cells plays an important role in the pathogenesis of hepatic reperfusion injury is supported, as well as analysis of liver tissue by electron paramagnetic resonance spectroscopy, providing direct evidence that carbon-centered radicals were generated on reflow.
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TLDR
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TLDR
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