Multiple-System Organ Damage Resulting From Prolonged Hepatic Inflow Interruption

Liu, David L.; Jeppsson, Bengt; Håkansson, C. H.; Odselius, Rolf

doi:10.1001/archsurg.1996.01430160100022

Cited by 130 publications

(94 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The severe damage associated with liver retrieval, preservation, and reperfusion often leads to primary graft nonfunction and may adversely affect the development of chronic rejection. [1][2][3] The response to hepatic I/R includes a cascade of Kupffer cell-derived proinflammatory mediators, activation of vascular endothelial cells, up-regulation of cellular adhesion molecules, and increased production of CXC chemokines. This results in adherence of neutrophils in hepatic microcirculation and transmigration into the liver parenchyma.…”

Section: T He Ischemia and Reperfusion (I/r) Syndrome Anmentioning

confidence: 99%

Stat4 and Stat6 signaling in hepatic ischemia/reperfusion injury in mice: HO-1 dependence of Stat4 disruption-mediated cytoprotection

Shen

2003

Hepatology

104

View full text Add to dashboard Cite

Section: T He Ischemia and Reperfusion (I/r) Syndrome Anmentioning

confidence: 99%

Stat4 and Stat6 signaling in hepatic ischemia/reperfusion injury in mice: HO-1 dependence of Stat4 disruption-mediated cytoprotection

Shen

2003

Hepatology

104

View full text Add to dashboard Cite

“…mitochondrial respiration; hepatocytes ISCHEMIA-REPERFUSION (I/R) injury is a major complication of transplantation, liver resection, and hemorrhagic shock (1,5,8,20,23). The injury resulting from warm hepatic I/R has a biphasic pattern.…”

mentioning

confidence: 99%

Peroxiredoxin-6 protects against mitochondrial dysfunction and liver injury during ischemia-reperfusion in mice

Eismann¹,

Huber²,

Shin³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

127

108

View full text Add to dashboard Cite

Hepatic ischemia-reperfusion (I/R) injury is an important complication of liver surgery and transplantation. Mitochondrial function is central to this injury. To examine alterations in mitochondrial function during I/R, we assessed the mitochondrial proteome in C57Bl/6 mice. Proteomic analysis of liver mitochondria revealed 234 proteins with significantly altered expression after I/R. From these, 13 proteins with the greatest expression differences were identified. One of these proteins, peroxiredoxin-6 (Prdx6), has never before been described in mitochondria. In hepatocytes from sham-operated mice, Prdx6 expression was found exclusively in the cytoplasm. After ischemia or I/R, Prdx6 expression disappeared from the cytoplasm and appeared in the mitochondria, suggesting mitochondrial trafficking. To explore the functional role of Prdx6 in hepatic I/R injury, wild-type and Prdx6-knockout mice were subjected to I/R injury. Prdx6-knockout mice had significantly more hepatocellular injury compared with wild-type mice. Interestingly, the increased injury in Prdx6-knockout mice occurred despite reduced inflammation and was associated with increased mitochondrial generation of H2O2 and dysfunction. The mitochondrial dysfunction appeared to be related to complex I of the electron transport chain. These data suggest that hepatocyte Prdx6 traffics to the mitochondria during I/R to limit mitochondrial dysfunction as a protective mechanism against hepatocellular injury.

show abstract

“…In animal models, an interruption of portal flow for up to 90 minutes results in increased permeability of the splanchnic vessels, interstitial edema of the gut, and the accumulation of acute inflammatory cells with evidence of mucosal cell damage. 16,17 With the release of portal clamping, inflammatory cytokines are released into the liver and subsequently the systemic circulation, leading to vasodilatation and end organ damage, including subpericardial hemorrhage, myocardial necrosis, and pulmonary infiltration and edema. 16,17 It has been postulated that a TPCS prevents splanchnic congestion and helps to maintain portal venous return, thereby abrogating the regional and systemic consequences associated with prolonged portal vein clamping.…”

Section: Discussionmentioning

confidence: 99%

Temporary portocaval shunt in orthotopic liver transplantation: Need for a standardized approach?

2008

View full text Add to dashboard Cite

Maintenance of portal and systemic venous return during the anhepatic phase of liver transplantation (LT) improves hemodynamic stability. With the piggyback technique, caval return is maintained; however, temporary clamping of the portal vein is still necessary. The use of a temporary portocaval shunt (TPCS) has been proposed to minimize the effect of portal venous interruption. The aim of this study was to perform a systematic review of the literature to determine whether there is evidence to support the routine use of a TPCS in LT. An electronic search of the literature from 1963 to 2007 was performed. A total of 4386 articles were identified, of which 8 met all the criteria and were included in the study. Because of the variability in reporting and the small number of studies, statistical comparison was not possible; however, a trend toward a shorter operative time, less blood product transfusion, and maintenance of higher mean arterial pressures during portal vein clamping was seen in patients with a TPCS. In conclusion, the available evidence, albeit scarce, supports the use of a TPCS in patients undergoing LT. A prospective randomized study of patients most likely to benefit from a TPCS is necessary to substantiate these findings.

show abstract

Multiple-System Organ Damage Resulting From Prolonged Hepatic Inflow Interruption

Cited by 130 publications

References 16 publications

Stat4 and Stat6 signaling in hepatic ischemia/reperfusion injury in mice: HO-1 dependence of Stat4 disruption-mediated cytoprotection

Stat4 and Stat6 signaling in hepatic ischemia/reperfusion injury in mice: HO-1 dependence of Stat4 disruption-mediated cytoprotection

Peroxiredoxin-6 protects against mitochondrial dysfunction and liver injury during ischemia-reperfusion in mice

Temporary portocaval shunt in orthotopic liver transplantation: Need for a standardized approach?

Contact Info

Product

Resources

About