A comparison of Collins and UW solutions for cold ischemic preservation of the rat liver

Sankary, Howard; Foster, Patricia L.; Brown, Esther; Hart, Michael H.; Williams, James W.

doi:10.1016/0022-4804(91)90075-w

Cited by 17 publications

(7 citation statements)

References 8 publications

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“…Bile flow and bile acid excretion, however, is a highly sensitive indicator of early graft function in human liver transplantation [8,9], which may depend on the activation state of KCs [24]. Therefore, by inhibition of KCs changes in hepatocellular function could be expected.…”

Section: Resultsmentioning

confidence: 99%

“…The IR‐injury in liver grafts is characterized by a sequence of morphologic changes. These include disturbances of microvascular perfusion secondary to injury of the sinusoidal lining signified by endothelial cells and Kupffer cell (KC) disturbances [5,6], intrahepatic accumulation of white blood cells (WBCs) [7], and impaired hepatocellular function [8,9]. In addition, apoptotic cell death has been acknowledged as an important mechanism related to cellular IR injury [5,10].…”

Section: Introductionmentioning

confidence: 99%

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Benefit of Kupffer cell modulation with glycine versus Kupffer cell depletion after liver transplantation in the rat: effects on postischemic reperfusion injury, apoptotic cell death graft regeneration and survival*

et al. 2005

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Summary Inhibition or destruction of Kupffer cells (KC) may protect against ischemia‐reperfusion (IR) induced primary graft nonfunction (PNF) in liver transplantation. Besides KC activation, PNF is characterized by microvascular perfusion failure, intrahepatic leukocyte accumulation, cell death and hepatocellular dysfunction. KCs can be inactivated by different agents including gadolinium chloride (GdCl3), methyl palmitate (MP) and glycine. The effects of three KC inactivators on IR‐injury after rat liver transplantation were compared in the present study. Lewis liver donors were treated with GdCl3, MP, glycine or saline (control). Liver grafts were transplanted following 24 h storage (UW solution). KC populations and IR damage were assessed by histologic analysis, quantitative real‐time polymerase chain reaction (RT‐PCR) and intravital microscopy. The number of hepatic ED‐1 positive macrophages was diminished after GdCl3 (114.8 ± 4.4/mm2 liver tissue) and MP treatment (176.0 ± 5.0), versus the glycine (263.9 ± 5.5) and control (272.1 ± 5.6) groups. All three treatment modalities downregulated phagocytic activity for latex particles, paralleled by reduced microvascular injury (acinar perfusion index, GdCl3: 0.75 ± 0.03; MP: 0.83 ± .03; glycine: 0.84 ± 0.03; 0.63 ± 0.03). Quantitative RT‐PCR revealed elevated myeloperoxidase mRNA after glycine versus GdCl3 and MP pretreatment (3.2‐ and 3.4‐fold, P = 0.011, respectively), without difference to controls (2.9‐fold of glycine). TNFα‐mRNA was reduced after glycine‐ (5.2‐fold), GdCl3‐ (19.7‐fold), MP‐treatment (39.5‐fold) compared with controls. However, profound prevention of intrahepatic cell death and liver graft failure was solely achieved with glycine preconditioning. Different than GdCl3 and MP, glycine modulates rather than destroys KCs. Glycine appears to preserve cell viability and to TNFα/leukocyte dependent organ regeneration capacity, which is related to increase graft survival following liver transplantation.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Benefit of Kupffer cell modulation with glycine versus Kupffer cell depletion after liver transplantation in the rat: effects on postischemic reperfusion injury, apoptotic cell death graft regeneration and survival*

et al. 2005

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“…On the other hand, however, several retrospective studies in human cases of liver transplantation as well as experimental investigations using rats indicated that the critical storage time that could trigger the risks is in a range between 12 and 18 hours. [27][28][29] In this context, to analyze experimentally early events in the graft damages that occur during these critical periods is still of great clinical importance.…”

Section: Discussionmentioning

confidence: 99%

Kupffer cell-independent acute hepatocellular oxidative stress and decreased bile formation in post-cold-ischemic rat liver

et al. 1999

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The purpose of this study was to examine distribution and time history of oxidative stress during the hyperacute period of reperfusion in the liver grafts undergoing cold ischemia and to investigate roles of Kupffer cells as a potential oxidant source. Rat livers were harvested at 4ЊC in University of Wisconsin solution and followed by reperfusion with Krebs-Henseleit buffer under monitoring bile excretion. To investigate oxidative changes, laser-confocal microfluorography was performed in reperfused livers preloaded with dichlorodihydrofluorescein diacetate succinimidyl ester, a fluorescence precursor sensing intracellular hydroperoxide generation. Livers undergoing the 16-hour cold storage displayed an impaired recovery of bile aciddependent bile output concurrent with a marked increase in hydroperoxide generation in hepatocytes, which occurred as early as 5 minutes after the onset of reperfusion, whereas the status of lobular perfusion was well maintained. Pretreatment with liposome-encapsulated dichloromethylene diphosphonate, a Kupffer cell-depleting reagent, did neither alter the reperfusion-induced periportal oxidative changes nor improve the recovery of bile output in the graft. On the other hand, EPCK, a hepatotropic antioxidant composed of vitamin E phosphate ester bound to vitamin C, not only diminished the oxidative changes but also improved the reduction of bile acid-dependent bile output. Furthermore, the reagent was capable of inhibiting H 2 O 2 -induced oxidative stress in cultured hepatocytes. These results suggest that hepatocytes constitute a major site of the oxidative insult triggered through Kupffer cell-independent mechanisms and serve as an important cellular component to be protected by antioxidant therapeutics.

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“…We have already demonstrated the expression of HSP using the same method, and we have reported that heat preconditioning of the graft improves the survival rate of rat liver transplants (16). It has also been reported in the rat transplantation model that the survival rate of transplanted animals drops significantly in the case of long-term preservation (>8 hr) in Euro-Collins solution (23). Thus, in our experiments, the 1-week survival rate for rats transplanted with livers that were preserved for 8 hr was 0% in the C group and 60% in the HP group.…”

Section: Discussionmentioning

confidence: 82%

Downregulation of Cytokine Release by Heat Preconditioning of Livers Used for Transplantation in Rats

et al. 2005

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We evaluated the changes in the levels of released cytokines following heat preconditioning of the livers used in rat liver transplantation. The donor rats in the heat preconditioning (HP) group were subjected to heat preconditioning 48 h before graft harvesting. The liver isografts were preserved in Euro-Collins solution for 8 h, and then transplanted orthotopically. The one-week survival rate of the HP group was significantly better than that of the control (C) group. The serum levels of interleukin-6 and interleukin-10 were significantly lower in the HP group than in the C group. Histological staining revealed that the stagnation of red blood cells and infiltration of neutrocytes were reduced in the HP group. The expression of intercellular adhesion molecule-1 was decreased around the central vein in the HP group, as revealed by immunohistochemistry. These results indicate that heat preconditioning downregulates cytokine release and reduces the frequency of microcirculation disorders.

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A comparison of Collins and UW solutions for cold ischemic preservation of the rat liver

Cited by 17 publications

References 8 publications

Benefit of Kupffer cell modulation with glycine versus Kupffer cell depletion after liver transplantation in the rat: effects on postischemic reperfusion injury, apoptotic cell death graft regeneration and survival*

Benefit of Kupffer cell modulation with glycine versus Kupffer cell depletion after liver transplantation in the rat: effects on postischemic reperfusion injury, apoptotic cell death graft regeneration and survival*

Kupffer cell-independent acute hepatocellular oxidative stress and decreased bile formation in post-cold-ischemic rat liver

Downregulation of Cytokine Release by Heat Preconditioning of Livers Used for Transplantation in Rats

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