• 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
        }
}
  • Z. Zhong, G. Arteel, +6 authors R. Thurman
  • Published 1 August 1999
  • Chemistry, Medicine
  • The Journal of pharmacology and experimental therapeutics
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… 
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21 Citations
Background Citations
7
Methods Citations
2

21 Citations

Citation Type

Citation Type

Polyphenols from Camellia sinenesis prevent primary graft failure after transplantation of ethanol-induced fatty livers from rats.
TLDR
In conclusion, polyphenols scavenged free radicals in ethanol-induced fatty livers and decreased injury after liver transplantation.
Role of free radicals in failure of fatty liver grafts caused by ethanol.
TLDR
It is indicated that free radicals increase in fatty grafts after transplantation and play an important role in injury of fatty grafting obtained from ethanol-exposed donors and treatment of fatty donor livers with antioxidants and free radical scavengers may thus be an effective clinical therapy to prevent failure of fat grafts.
ICAM-1 Upregulation in Ethanol-Induced Fatty Murine Livers Promotes Injury and Sinusoidal Leukocyte Adherence after Transplantation
TLDR
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.
Role of inducible nitric oxide synthase in mitochondrial depolarization and graft injury after transplantation of fatty livers.
TLDR
iNOS is upregulated after transplantation of FG, leading to excessive RNS formation, JNK activation, mitochondrial dysfunction, and severe graft injury, and the iNOS inhibitor 1400W could be an effective therapy for primary nonfunction of fatty liver grafts.
Ischemia-reperfusion Injury after Canine Liver Allo-transplantation: The Effect of Gadolinium Chloride.
TLDR
Kupffer cell blockage using the Gadolinium chloride might be an effective way of reducing ischemia reperfusion injury, however, this effect was not evident in the early stages of reperfusions.
Kupffer cell inactivation alleviates ethanol-induced steatosis and CYP2E1 induction but not inflammatory responses in rat liver.
TLDR
Gadolinium chloride reduces symptoms of ALD mainly by counteracting steatosis, and that CD14-positive Kupffer cell populations are not involved in gadolinium protection.
Repeated whiskey binges promote liver injury in rats fed a choline-deficient diet.
TLDR
Repeated alcohol binges in the context of mild steatosis may promote activation of stellate cells and contribute to liver injury in this model of liver injury.
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.
Acute alcohol intoxication and gadolinium chloride attenuate endotoxin-induced release of CC chemokines in the rat.
TLDR
Data show that acute ethanol may be beneficial in tissue injury during acute endotoxemia, and suppressed the LPS-mediated priming of Kupffer cells for enhanced CC-chemokine release in vitro.
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

SHOWING 1-10 OF 49 REFERENCES
Destruction of Kupffer cells increases survival and reduces graft injury after transplantation of fatty livers from ethanol-treated rats.
  • Z. Zhong, H. Connor, +5 authors R. Thurman
  • Medicine
    Liver transplantation and surgery : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society
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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.
Antibiotics prevent liver injury in rats following long-term exposure to ethanol.
TLDR
Intestinal sterilization prevented alcohol-induced liver injury in the rat, supporting the idea that hypermetabolism and consequent hypoxia caused by activation of Kupffer's cells by endotoxin is involved in the mechanism.
Primary nonfunction of fatty livers produced by alcohol is associated with a new, antioxidant-insensitive free radical species.
TLDR
Both dietary high fat and alcohol exposure produce a unique SOD/catalase-insensitive free radical species that may be involved in the mechanism of failure of fatty livers after orthotopic liver transplantation.
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TLDR
Data indicate that the ethanol-induced hepatic vasoconstriction disturbs hepatic microcirculation, resulting in hepatic hypoxia and reduction of mitochondrial respiratory cytochromes.
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TLDR
The hypothesis that a brief rinse of liver grafts with warm buffer markedly improves the hepatic microcirculation, leading to dramatic improvement in graft survival is supported, and a brief warm rinse may be useful clinically in liver transplantation is demonstrated.
Ethanol, not fat accumulation per se, increases free radical production in a low-flow, reflow liver perfusion model.
TLDR
Ethananol plays a major role in hepatic reperfusion injury, most likely via mechanisms involving free radicals, and increased hepatic fat content alone plays only a minor role, probably by causing slight disturbances in the hepatic microcirculation.
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TLDR
Kupffer cells isolated from rats early after ethanol exhibited tolerance to LPS, whereas sensitization was observed later, suggesting that both of these phenomena are caused by gut-derived endotoxin and that sensitization in K upffer cells is caused by increases in CD14.
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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.
Evidence that graft survival is not related to parenchymal cell viability in rat liver transplantation. The importance of nonparenchymal cells.
TLDR
Although parenchymal cell function was in the normal range in livers stored in the cold for 24 hr, liver grafts stored for 6 hr and longer in Euro-Collins solution could not be transplanted successfully and it is concluded that viability of paren chymal cells in liver grafting prior to transplantation is a poor parameter to predict the outcome of transplantation.
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TLDR
The results of this study demonstrate the existence of two distinct mechanisms of adhesion, one operative after harvesting and a short period of preservation and another operative after longer periods, as well as the possible presence of mechanical obstruction.
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