Destruction of Kupffer’s cells increases total liver blood flow and decreases ischemia reperfusion injury in pigs

Frankenberg, Moritz von; Golling, M.; Mehrabi, Arianeb; Nentwich, Hagen; Thies, Jochen; Schaeffer, F; Jahnke, Cosima; Bud, Octavian; Gebhard, Martha Maria; Otto, Gerd; Thurman, Ronald G.; Herfarth, Ch.; Klar, E.

doi:10.1016/s0041-1345(99)00714-9

Cited by 9 publications

(2 citation statements)

References 3 publications

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“…Conversely, depletion of Kupffer cells significantly ameliorates the microcirculatory perturbations of trauma and sepsis [48]. In accord with these findings, Kupffer's cell depletion led to a strong effect on portal and arterial blood flow, with an > 50% increase in total liver blood flow following liver transplantation in pigs [49]. Kupffer cells are known to express a variety of vasoregulatory enzyme systems with the release of vasoactive mediators, including endothelins, ROS, NO and prostanoids, which can cause changes in endothelial cells and activation and contraction of hepatic stellate cells (HSC) [22].…”

Section: Inflammation and Fibrosismentioning

confidence: 64%

Non-alcoholic fatty liver disease, to struggle with the strangle: Oxygen availability in fatty livers

2017

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Nonalcoholic fatty liver diseases (NAFLD) is one of the most common chronic liver disease in Western countries. Oxygen is a central component of the cellular microenvironment, which participate in the regulation of cell survival, differentiation, functions and energy metabolism. Accordingly, sufficient oxygen supply is an important factor for tissue durability, mainly in highly metabolic tissues, such as the liver. Accumulating evidence from the past few decades provides strong support for the existence of interruptions in oxygen availability in fatty livers. This outcome may be the consequence of both, impaired systemic microcirculation and cellular membrane modifications which occur under steatotic conditions. This review summarizes current knowledge regarding the main factors which can affect oxygen supply in fatty liver.

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Section: Inflammation and Fibrosismentioning

confidence: 64%

Non-alcoholic fatty liver disease, to struggle with the strangle: Oxygen availability in fatty livers

2017

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“…However, the results remain controversial. Some investigators showed that Kupffer cell inhibition prevented endothelial cell deterioration 30 and microcirculatory disturbances, 21,31,32 improved blood flow, 33 and ameliorated graft survival. 13,31,32 Conversely, others failed to show an effect of Kupffer cell blockade on hepatocyte damage during preservation, 24 on functions of hepatocytes 20,21,34 and sinusoidal endothelial cells 20,34 during reperfusion, or on graft survival.…”

Section: Is Deterioration Of Liver Microcirculation Exclusively Respomentioning

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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Konditionierung vor warmer Leberischämie durch Kupfferzellblockade — Effekte auf Leber, Niere, Herz und Lunge

Frankenberg

Weimann

Alsfasser

et al. 2001

Deutsche Gesellschaft Für Chirurgie

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Destruction of Kupffer’s cells increases total liver blood flow and decreases ischemia reperfusion injury in pigs

Cited by 9 publications

References 3 publications

Non-alcoholic fatty liver disease, to struggle with the strangle: Oxygen availability in fatty livers

Non-alcoholic fatty liver disease, to struggle with the strangle: Oxygen availability in fatty livers

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

Konditionierung vor warmer Leberischämie durch Kupfferzellblockade — Effekte auf Leber, Niere, Herz und Lunge

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