Primary graft dysfunction after liver transplantation: From pathogenesis to prevention

Bzeizi, Khalid; Jalan, Rajiv; Plevris, John; Hayes, Peter

doi:10.1002/lt.500030206

Cited by 79 publications

(28 citation statements)

References 68 publications

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“…However, we also found no difference in various indices of graft function in a larger retrospective analysis comparing the two methods of reperfusion. 6 Differences in the portal venous and hepatic arterial circulations could explain our observations. The portal venous system is a high-flow, low-pressure, low-resistance circulation that drains directly into hepatic sinusoids, from which oxygen diffuses to hepatocytes.…”

mentioning

confidence: 67%

“…In our previous study, we calculated that approximately 300 patients would require randomization to test the hypothesis that the techniques have similar outcomes. 6 Metabolic measurements were made using a metabolic monitor that measures VCO, directly, but makes some assumptions in deriving VO,. These relate mainly to steady state for nitrogen and carbon dioxide in the body.'…”

Section: Discussionmentioning

confidence: 99%

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Metabolic, cardiovascular, and acid-base status after hepatic artery or portal vein reperfusion during orthotopic liver transplantation

Walsh

Garden

Lee

2002

Liver Transplantation

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During liver transplantation, reperfusion traditionally is performed through the portal vein. After anecdotal observations that patients who underwent reperfusion first through the hepatic artery were more hemodynamically stable, we performed an exploratory, prospective, observational, nonrandomized study to compare cardiovascular stability, acid-base status, and metabolic gas exchange between patients who underwent reperfusion through either the portal vein or hepatic artery. We studied 20 patients undergoing liver transplantation (10 patients, reperfusion first through the portal vein; 10 patients, reperfusion first through the hepatic artery). Cardiovascular and acid-base parameters were compared at times before and after anastomosis of each vessel, and epinephrine use was recorded. Oxygen consumption (VO,) and carbon dioxide elimination (VCO,) were measured continuously by using an indirect calorimeter. Alanine aminotransferase (WT) concentrations 24 hours after transplantation were compared as an index of reperfusion injury. Cardiovascular changes (mean arterial pressure, cardiac output) were similar for both groups, but more epinephrine was administered to the portal-vein group (P = .014). There was a greater increase in Paco, after portal reperfusion (median portal vein, 1.01 m a ; hepatic artery, 0.29 Wa; P = ,015) and a trend toward more severe acidemia. Vo, increased more rapidly in the portalvein group (P = .005), but overall changes in VO, during the study period were similar. There were no differences in Vco, between the groups or ALT concentrations 24 hours posttransplantation. These observational data suggest that hepatic arterial reperfusion may be associated with reduced epinephrine requirements and a slower rate of acid release, which could be advantageous in unstable patients. VO, increases more slowly after hepatic artery reperfusion, which could indicate slower reoxygenation of the graft. 537-544.)D uring liver transplantation, the period of greatest patient instability is often after graft reperfusion. Reperfusion can affect patients through two processes that can be considered immediate and delayed. Immediate effects include alterations in cardiovascular, metabolic, and acid-base states that occur within minutes of vascular reperfusion. Delayed effects may not be apparent for 24 to 48 hours and result from reperfusion injury to the graft itself.' Reperfusion injury is initiated at the time of vascular reperfusion and characterized by endothelial and Kupffer's cell injury in hepatic sinuLiver Transplantation, Vol8, soids, reduction in blood flow through these vessels, and hepatocyte damage.2 Ischemia-reperfusion injury can result in significant graft dysfunction in the postoperative period.The ideal technique for graft reperfusion should minimize both immediate and delayed complications. Reperfusion usually is performed through the portal vein as soon as this anastomosis is complete, followed by the hepatic artery. The origin of this practice appears to be largely historical, originating f...

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mentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Metabolic, cardiovascular, and acid-base status after hepatic artery or portal vein reperfusion during orthotopic liver transplantation

Walsh

Garden

Lee

2002

Liver Transplantation

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“…3 ), thus preventing hepatic microcirculation disturbances ( table 1 ). One possible explanation for microcirculation disturbances following warm ischemia/reperfusion concerns the production of TNF-␣ which leads to an enhanced production and liberation of endothelin-1 (ET-1) [41] . ET-1 itself has an ef- fect on the smooth muscle cells of arteries and venules as well as on the contractile Ito cells [42] .…”

Section: Discussionmentioning

confidence: 99%

Taurine Protects from Liver Injury after Warm Ischemia in Rats: The Role of Kupffer Cells

et al. 2007

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Background/Aims: Warm ischemia to liver with subsequent Kupffer cell-dependent pathology is associated with many clinical conditions. Taurine prevents Kupffer cell activation and improves graft survival after experimental cold ischemia and liver transplantation. Thus this study was designed to assess its effects after warm hepatic ischemia. Methods: The left liver lobe of female Sprague-Dawley rats (170–210 g) underwent 60 min of warm ischemia. Animals were given either intravenous taurine or Ringer’s solution 10 min prior to warm ischemia. Transaminases, histology, in vivo microscopy, intercellular adhesion molecules-1 (ICAM-1) expression, TNF-α and tissue hydroperoxide were compared between groups using analysis of variance (ANOVA) or ANOVA on ranks as appropriate. Results: Taurine significantly decreased transaminases and improved histologic outcome. Phagocytosis of latex beads, serum TNF-α levels and tissue hydroperoxide concentrations were also significantly reduced. Stickers in sinusoids and post-sinusoidal venules significantly decreased. In parallel, both leukocyte infiltration and ICAM-1 expression decreased (p < 0.05), while flow velocity of red blood cells as well as sinusoidal perfusion rate were improved (p < 0.05). Conclusion: This study demonstrates that taurine blunts Kupffer cell-dependent hepatic pathology after warm ischemia in vivo via mechanisms including leukocyte-endothelial interaction, microcirculation disturbances and protection against lipid peroxidation.

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“…Die Vorteile der Lebendlebertransplantation liegen in einer niedrigeren Inzidenz an primärem Organversagen (primary craft dysfunction). Die Abstoßungsreaktion scheint verglichen mit Kadaverorganen gleich häufig aber dafür weniger stark aufzutreten [10].…”

Section: Lebendleberspendeunclassified

Anaesthesie zur Organentnahme

Sinner

2002

Der Anaesthesist

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Primary graft dysfunction after liver transplantation: From pathogenesis to prevention

Cited by 79 publications

References 68 publications

Metabolic, cardiovascular, and acid-base status after hepatic artery or portal vein reperfusion during orthotopic liver transplantation

Metabolic, cardiovascular, and acid-base status after hepatic artery or portal vein reperfusion during orthotopic liver transplantation

Taurine Protects from Liver Injury after Warm Ischemia in Rats: The Role of Kupffer Cells

Anaesthesie zur Organentnahme

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