Influence of donor condition on postoperative graft survival and function in human liver transplantation

Totsuka, Eishi; Fung, John J.; Ishii, Tomohiro; Urakami, Atsushi; Moras, Natalia; Hakamada, Kenichi; Narumi, S.; Watanabe, Noboru; Nara, Masaki; Hashimoto, Naoki; Takiguchi, M; Nozaki, Tomoyoshi; Umehara, Yutaka; Sasaki, Mutsuo

doi:10.1016/s0041-1345(99)00969-0

Cited by 25 publications

(14 citation statements)

References 10 publications

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“…71,72 Such treatment often results in hypernatremia, which is associated with an increased risk of graft dysfunction after liver transplantation. [73][74][75] Another effect of this osmotherapy is that it may slow down the herniation process, leading to a less pronounced sympathetic storm with less damage to solid organs and probably less immunological activation. 28 …”

Section: Donor Managementmentioning

confidence: 99%

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Brain death and its implications for management of the potential organ donor

Bugge

2009

Acta Anaesthesiol Scand

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The systemic physiologic changes that occur during and after brain death affect all organs suitable for transplantation. Major changes occur in the cardiovascular, pulmonary, endocrine, and immunological systems, and, if untreated may soon result in cardiovascular collapse and somatic death. Understanding these complex physiologic changes is mandatory for developing effective strategies for donor resuscitation and management in such a way that the functional integrity of potentially transplantable organs is maintained. This review elucidates these physiological changes and their consequences, and based on these consequences the rationale behind current medical management of brain-dead organ donors is discussed.

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Section: Donor Managementmentioning

confidence: 99%

“…Administration of packed red cells to keep the hemoglobin level 100 g/l (or the hematocrit 30%) is recommended, 21,83 but is not evidence based. Hypernatremia should be corrected to avoid liver graft dysfunction, [73][74][75] and it also seems reasonable to correct other electrolyte abnormalities.…”

Section: Hemodynamic Managementmentioning

confidence: 99%

Brain death and its implications for management of the potential organ donor

Bugge

2009

Acta Anaesthesiol Scand

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“…Elevations usually last from several hours to approximately 2 days, and levels normalize within 1 week. 23 By contrast, reperfusion injury to the graft biliary tree, reflected by serum gamma-glutamyl transferase and bilirubin levels, persists for up to 17 days. 24 Histologically, the diagnosis of preservation-reperfusion injury is based on the presence of steatosis, cholestasis, and ballooning degeneration of hepatocytes in early posttransplantation biopsies 25 ( Fig.…”

Section: Early Intrahepatic Cholestatic Syndrome Ischemia/reperfusionmentioning

confidence: 99%

Intrahepatic cholestasis after liver transplantation

Ben‐Ari

Pappo

Mor

2003

Liver Transplantation

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Cholestasis is a common sequela of liver transplantation. Although the majority of cases remain subclinical, severe cholestasis may be associated with irreversible liver damage, requiring retransplantation. Therefore, it is essential that clinicians be able to identify and treat the syndromes associated with cholestasis. In this review, we consider causes of intrahepatic cholestasis. These may be catego-

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“…168,169 Donor hypernatremia is associated with graft dysfunction in clinical liver transplantation, whereas correction of hypernatremia before liver procurement improves graft function. 170 Finally, platelets and platelet-activating factor have been implicated in microcirculatory disturbances and liver injury after transplantation. 171,172 However, using a bloodfree perfusion model, Hashikura et al 173 showed that platelet-activating factor acting on hepatocytes impaired ATP synthesis and aggravated hepatic graft dysfunction, even in the absence of microcirculatory disturbances.…”

Section: Increased Sensitivity Of Hepatocyte Functions To Various Stimentioning

confidence: 99%

“…170 Plasma levels of these enzymes usually normalize within one week. Conversely, reperfusion injury to the graft biliary tree persists for a much longer period.…”

Section: Bile Duct Cell Injury: Long-lasting Phase Of Reperfusion Injurymentioning

confidence: 99%

Role of hepatocytes and bile duct cells in preservation-reperfusion injury of liver grafts

Kukan

Haddad

2001

Liver Transplantation

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In liver transplantation, it is currently hypothesized that nonparenchymal cell damage and/or activation is the major cause of preservation-related graft injury. Because parenchymal cells (hepatocytes) appear morphologically well preserved even after extended cold preservation, their injury after warm reperfusion is ascribed to the consequences of nonparenchymal cell damage and/or activation. However, accumulating evidence over the past decade indicated that the current hypothesis cannot fully explain preservation-related liver graft injury. We review data obtained in animal and human liver transplantation and isolated perfused animal livers, as well as isolated cell models to highlight growing evidence of the importance of hepatocyte disturbances in the pathogenesis of normal and fatty graft injury. Particular attention is given to preservation time-dependent decreases in high-energy adenine nucleotide levels in liver cells, a circumstance that (1) sensitizes hepatocytes to various stimuli and insults, (2) correlates well with graft function after liver transplantation, and (3) may also underlie the preservation timedependent increase in endothelial cell damage. We also review damage to bile duct cells, which is increasingly being recognized as important in the long-lasting phase of reperfusion injury. The role of hydrophobic bile salts in that context is particularly assessed. Finally, a number of avenues aimed at preserving hepatocyte and bile duct cell integrity are discussed in the context of liver transplantation therapy as a complement to reducing nonparenchymal cell damage and/or activation. (Liver Transpl 2001;7: 381-400.)A lthough the use of University of Wisconsin (UW) solution has permitted an increase in mean preservation time, the incidence of graft dysfunction still persists, 1,2 contributing significantly to a more than 20% per year mortality rate for patients in liver transplantation centers in the United States. 3 In addition, when storage time exceeds 10 to 12 hours, such late posttransplantation complications as biliary strictures occur in more than 25% of liver transplant recipients. [4][5][6] To prevent or minimize graft dysfunction and posttransplantation complications, it is essential to fully understand the importance of individual liver cell types in graft injury induced by cold storage and reperfusion. Insight into the cellular and molecular basis of these injuries will lead to the development of better intervention strategies, which is very important because graft dysfunction results in increased morbidity and enhances mortality rates. 7,8 Moreover, up to 30% of patients with graft dysfunction need retransplantation as early as within the first 3 months after transplantation, 2,7,8 which increases the demand on an already short pool of donor organs.According to morphological studies, cold preservation leads to injuries of nonparenchymal cells, whereas liver parenchymal cells appear well preserved. It is currently hypothesized that sinusoidal endothelial cell impairment, 9-11 activatio...

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Influence of donor condition on postoperative graft survival and function in human liver transplantation

Cited by 25 publications

References 10 publications

Brain death and its implications for management of the potential organ donor

Brain death and its implications for management of the potential organ donor

Intrahepatic cholestasis after liver transplantation

Role of hepatocytes and bile duct cells in preservation-reperfusion injury of liver grafts

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