Livers From Fasted Rats Acquire Resistance to Warm and Cold Ischemia Injury

Sumimoto, Ryo; Jh, Southard; Fo, Belzer

doi:10.1097/00007890-199304000-00008

Cited by 69 publications

(43 citation statements)

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“…Interestingly, there are a few studies, using the ORLT model after cold preservation for 24 hours or more in the UW solution, that reported good survivals while also reporting a short PVCT (less than 13 minutes), 14,33,34 while PVCTs longer than 18 minutes were associated with poor outcomes. 13,35 These results are well in line with our findings.…”

Section: Discussionmentioning

confidence: 99%

Decreased survival in rat liver transplantation with extended cold preservation: Role of portal vein clamping time

Urata¹,

Nguyen²,

Brault³

et al. 1998

Hepatology

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Primary liver graft dysfunction is currently related to cold ischemia-reperfusion injury, although a wide survival range has been reported using 24-hour preservation in cold University of Wisconsin (UW) solution. We hypothesized that the portal vein clamping time (PVCT) played a more important role than cold preservation injury in the postoperative outcome. Rat liver transplantation was performed using different clamping times after 24-hour cold ischemia in the UW solution. Survival rates, plasma tumor necrosis factor (TNF), and nitrate/nitrite levels were examined. Subsequently, the effect of clamping time was evaluated on hepatocyte and sinusoidal endothelial cell (SEC) function using isolated perfused livers. Survival rate was directly related to clamping time length. Marked increases in TNF and nitrate/nitrite levels were found after surgery, particularly after long clamping times. In perfusion studies, the SEC function was already markedly altered after preservation alone and was not further modified by transplantation. By contrast, the hepatocyte function was moderately altered after transplantation, irrespective of clamping times, even when rats operated with long clamping times were in terminal conditions. In rats, 24-hour preservation in cold UW solution is not a severely compromising condition leading to primary liver nonfunction. Long PVCTs are associated with an endotoxemia-like syndrome more related to a warm intestinal ischemia than to cold ischemia injury of the liver. (HEPATOLOGY 1998;28:366-373.)The underlying mechanism of cold ischemia-reperfusion injury of the liver culminating in primary liver nonfunction is still poorly understood. It is currently hypothesized that Kupffer cell activation plays a causal role in cold ischemiareperfusion injury of the liver, precipitating sinusoidal endothelial cell (SEC) death, and leading to microcirculatory disturbances. [1][2][3][4][5][6][7] This hypothesis is based on experimental findings using mainly the orthotopic rat liver transplantation (ORLT) model, first described by Lee et al. 8 and subsequently modified by Kamada and Calne. 9 However, recent experimental reports have shown that, after ORLT following extended cold ischemia, the mortality of animals could not be related to the severity of SEC dysfunction. 10 Moreover, Imamura et al. 11 and Reinders et al. 12 have reported that the presence or absence of Kupffer cells did not modify the effect of 24-hour cold ischemia/ reperfusion using the isolated perfused rat liver model and/or the ORLT model.Indeed, the ORLT model has been widely used for studying cold ischemia-reperfusion injury of the liver, particularly the effects of various solutions and of different biochemical strategies aimed at protecting the transplanted liver. A large number of these studies used cold University of Wisconsin (UW) solution as the preservation solution and 24 hours as the preservation time, conditions considered severely compromising for the grafted rat liver. However, under these preservation conditions, reported su...

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Section: Discussionmentioning

confidence: 99%

Decreased survival in rat liver transplantation with extended cold preservation: Role of portal vein clamping time

Urata¹,

Nguyen²,

Brault³

et al. 1998

Hepatology

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“…Extensive injury to nonparenchymal cells, such as endothelial cells, rather than damage to parenchymal cells during cold preservation, was shown ultrastructurally with rat livers [8,15]. In addition, nutritional status of donors [2,16,22] and warm ischemia during procurement or liver replacement [7,10] may influence initial graft function in human livers.…”

Section: Discussionmentioning

confidence: 99%

Can adenine nucleotides predict primary nonfunction of the human liver homograft?

et al. 1994

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“…Rats were fasted for 48 hours to deplete liver glycogen by 95%. 33 Livers were then cold stored in the UW solution for 48 hours. Total phospholipids decreased by 15% (from 0.196 Ϯ 0.003 µmole P/mg protein to 0.167 Ϯ 0.001 µmole P/mg protein).…”

Section: Role Of Pla 2 In Degradation Of Membrane-bound Phospholipids Inmentioning

confidence: 99%

Phospholipid metabolism of hypothermically stored rat hepatocytes

Kim

Southard

1999

Hepatology

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Livers From Fasted Rats Acquire Resistance to Warm and Cold Ischemia Injury

Cited by 69 publications

References 0 publications

Decreased survival in rat liver transplantation with extended cold preservation: Role of portal vein clamping time

Decreased survival in rat liver transplantation with extended cold preservation: Role of portal vein clamping time

Can adenine nucleotides predict primary nonfunction of the human liver homograft?

Phospholipid metabolism of hypothermically stored rat hepatocytes

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