Long-term cold liver storage induces endothelin-1 release and a time-dependent increase in portal pressure at reperfusion in the rat

Charrueau, Christine; Carayon, A.; Thurman, Ronald G.

doi:10.1007/s005350200117

Cited by 14 publications

(8 citation statements)

References 45 publications

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“…Other factors directly influencing the width of the perfused sinusoids have to be considered as well; e.g., the regulation of the endothelin A (ET A )/endothelin B (ET B ) receptor ratio under I/R conditions which results in a ET B ‐mediated NO release and sinusoidal relaxation, although this is not analyzed within this study. Finally, studies utilizing FITC‐dextran fluorescence measurements23, 24 or laser Doppler flowmetry9 confirm the aforementioned hyperemia on the liver surface following cold ischemia and subsequent reperfusion.…”

Section: Discussionmentioning

confidence: 90%

Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation

et al. 2005

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Microcirculatory disturbances are an initial causative determinant in hepatic ischemia/reperfusion injury. The aim of this study was to assess sinusoidal perfusion during human liver transplantation using orthogonal polarization spectral imaging and to evaluate the significance of intraoperative microcirculation for early postoperative graft function. Hepatic microcirculation was measured in 27 recipients undergoing full-size liver transplantation and compared to a group of 32 healthy living-related liver donors. The microvascular parameters were correlated with postoperative aspartate aminotransferase and bilirubin levels. Hepatic perfusion following liver transplantation was found to be significantly decreased when compared with the control group.

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Section: Discussionmentioning

confidence: 90%

Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation

et al. 2005

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“…It has become evident that during the early reperfusion that follows extended cold ischemia, the liver exhibits aberrant circulatory properties. The portal venous pressure increases dramatically, and oxygen consumption significantly decreases 32. Many of the sinusoidal channels are unperfused, endothelial cell apoptosis is enhanced,33 with retraction and detachment of cell bodies progressing to denudation of the sinusoidal lining,34 as well as the imbalance of vasoconstrictor/vasodilator molecules 35, 36.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory responses in a new mouse model of prolonged hepatic cold ischemia followed by arterialized orthotopic liver transplantation

Shen

Gao

et al. 2005

Liver Transpl

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The current models of liver ischemia/reperfusion injury (IRI) in mice are largely limited to a warm ischemic component. To investigate the mechanism of hepatic "cold" IRI, we developed and validated a new mouse model of prolonged cold preservation followed by syngeneic orthotopic liver transplantation (OLT). Two hundred and forty-three OLTs with or without rearterialization and preservation in University of Wisconsin solution at 4°C were performed in Balb/c mice. The 14-day survivals in the nonarterialized OLT groups were 92% (11/12), 82% (9/11), and 8% (1/12) after 1-hour, 6-hour and 24-hour preservation, respectively. In contrast, hepatic artery reconstruction after 1-hour, 6-hour, and 24-hour preservation improved the outcome as evidenced by 2-week survival of 100% (12/12), 100% (10/10), and 33% (4/12), respectively, and diminished hepatocellular damage (serum alanine aminotransferase /histology). Moreover, 24-hour (but not 1-h) cold preservation of rearterialized OLTs increased hepatic CD4؉ T-cell infiltration and proinflammatory cytokine (tumor necrosis factor-␣, interleukin 2, interferon-␥) production, as well as enhanced local apoptosis, and Toll-like receptor 4/caspase 3 expression. These cardinal features of hepatic IRI validate the model. In conclusion, we have developed and validated a new mouse model of IRI in which hepatic artery reconstruction was mandatory for long-term animal survival after prolonged (24-h) OLT preservation. With the availability of genetically manipulated mouse strains, this model should provide important insights into the mechanism of antigen-independent hepatic IRI and help design much needed refined therapeutic means to combat hepatic IRI in the clinics. (Liver Transpl 2005; 11:1273-1281.)

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“…Bile output was measured gravimetrically in prepared tubes. Portal pressure was monitored manometrically from tubing attached to the inflow (Charrueau et al, 2002). As an index of parenchymal cell injury, LDH activity in the perfusate was determined by standard spectrophotometric procedures by ChemiLab LDH assay kit (IVDLab Co.).…”

Section: Liver Weight To Body Weight Ratio and Hepatic Triglyceride Cmentioning

confidence: 99%

Protective effect of heme oxygenase-1 induction against hepatic injury in alcoholic steatotic liver exposed to cold ischemia/reperfusion

Kim¹,

Park²,

Lee³

2012

Life Sciences

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Long-term cold liver storage induces endothelin-1 release and a time-dependent increase in portal pressure at reperfusion in the rat

Abstract: Cold storage induces a time-dependent elevated portal pressure at reperfusion. The involvement of endothelin-1 in this process offers opportunities to improve liver graft quality by using endothelin-1 inhibitors.

Cited by 14 publications

References 45 publications

Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation

Initial hepatic microcirculation correlates with early graft function in human orthotopic liver transplantation

Inflammatory responses in a new mouse model of prolonged hepatic cold ischemia followed by arterialized orthotopic liver transplantation

Protective effect of heme oxygenase-1 induction against hepatic injury in alcoholic steatotic liver exposed to cold ischemia/reperfusion

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