Experimental Liver Preservation with Celsior:A Novel Alternative to University of Wisconsin and Histidine-Tryptophan-α-Ketoglutarate Solutions?

Tolba, René; Akbar, S; Müller, A.R; Glatzel, U; Minor, Thomas

doi:10.1159/000008755

Cited by 24 publications

(21 citation statements)

References 25 publications

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“…This was verified by our data from LDH release and MTT reduction. In contrast to data from a study with CS in a rat liver-transplantation model, our results from intracellular ATP failed to confirm a significantly higher level after the ischemia phase [36]. However, the results of ATP level after a consecutive reperfusion phase were in accordance with this rat-liver model and another recently performed study from pig-liver transplantation [2].…”

Section: Discussioncontrasting

confidence: 99%

Celsior solution compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK) in the protection of human hepatocytes against ischemia-reperfusion injury

Janssen¹,

Janbetaen²,

Broelsch³

2003

Transplant Int

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Celsior, a new preservation solution in thoracic organ transplantation was evaluated for efficacy in cold preservation of human hepatocytes and compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK, Custodiol). Human hepatocyte cultures were preserved at 4 "C in Celsior, UW and HTK for 2, 6, 12, 24 and 48 h with 6 h of reperfusion. Levels of lactate dehydrogenase (LDH; cell necrosis), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT; mitochondria1 function), and adenosine 5'-triphosphate (ATP; loss of intracellular energy) were measured. Cell necrosis, mitochondrial dysfunction, and loss of ATP were significantly (P < 0.001, P < 0.001, P < 0.002, respectively) lower in Celsior than in HTK. The amount of cell necrosis and mitochondrial dysfunction in Celsior solution (CS) and UW was equal (P = n.s.) up to 24 h and significantly lower in UW after 48 h (P< 0.001).Additionally, the intracellular level of ATP was significantly higher after ischemia (P < 0.001) and reperfusion from long-term ischemia (24, 48 h) (P < 0.002). We can conclude that Celsior was superior to HTK and equal to UW in the protection of human hepatocytes against cold preservation injury from ischemia and reperfusion. Furthermore, Celsior was effective in long-term preservation of human hepatocytes.

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Section: Discussioncontrasting

confidence: 99%

Celsior solution compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK) in the protection of human hepatocytes against ischemia-reperfusion injury

Janssen¹,

Janbetaen²,

Broelsch³

2003

Transplant Int

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“…Tissue MDA was extracted at 4 ° C in 10 ml/g dry weight (see above) of 0.33 mol/l perchloric acid (HClO 4 ) and then neutralized with 2 mol/l potassium hydroxide. After removing precipitated KClO 4 , the MDA concentrations were determined using a fluorometric method, as detailed elsewhere [22] .…”

Section: Tissue Lipid Peroxidationmentioning

confidence: 99%

A Natural Tetrahydropyrimidine Protects Small Bowel from Cold Ischemia and Subsequent Warm in vitro Reperfusion Injury

Wei¹,

Wedeking²,

Büttner

et al. 2009

Pathobiology

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Objective: Ischemia/reperfusion (I/R) injury is a major difficulty in small bowel transplantation. Many postoperative complications are caused by damage to the intestinal mucosa following organ retrieval and during cold storage. Here we investigate whether 1-, 4-, 5-, 6-tetrahydro-2-methyl-4-pyrimidine carboxylic acid (THP) can protect ileal mucosa and muscularis against cold ischemia and subsequent warm in vitro reperfusion injury. Methods: Small rat bowels were stored in the absence or presence of THP or its synthetic derivative lauryl-THP for 18 h at 4°C. Several biochemical parameters were evaluated following isolated reperfusion in tissue grafts and/or effluent solution. Graft morphology was analyzed by electron microscopy. Ceramide was quantified as a potential target of THP action. Results: THP considerably inhibited apoptosis and improved all parameters illustrating membrane and subcellular integrity and functionality. Parallel studies with lauryl-THP failed to show a similar protective effect. Lauryl-THP, in contrast to THP, also failed to decrease tissue ceramide content, indicating the involvement of this well-known mediator of cellular stress response. Conclusions: THP effectively protects ileal mucosa and muscularis against ischemia and reperfusion injury, indicating for the first time the clinical relevance of this new and promising molecule that might become a central component in tissue and organ protection in the near future.

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“…We obtained UW from DuPont (Bad Homburg, Germany), and HTK from Dr. Köhler Chemie GmbH (Alsbach, Germany) as described elsewhere [9].…”

Section: Preservation Solutionsmentioning

confidence: 99%

Value of Energy Substrates in HTK and UW to Protect Human Liver Endothelial Cells against Ischemia and Reperfusion Injury

Janssen¹,

Janssen²,

Broelsch³

2004

Eur Surg Res

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Adenosine 5′-triphosphate (ATP) depletion is a major cause of cellular injury during ischemia and reperfusion in organ transplantation. Therefore, histidine-tryptophan-ketoglutarate solution (HTK; α-ketoglutarate) and University of Wisconsin solution (UW; adenosine) were supplied with energy substrates to achieve graft viability. Nevertheless, their efficacy for maintaining the ATP level, particularly in human liver endothelial cells, was uncertain. Furthermore, it is of interest whether a high ATP level is beneficial in human liver endothelial cell viability. We used human liver endothelial cells between the 3rd and 6th passages in a cell culture model. Human liver endothelial cells were exposed to hypothermic preservation (4°C) in HTK and UW for 2, 6, 12, 24 and 48 h with subsequent reperfusion of 6 h. ATP and lactate dehydrogenase (LDH) were measured after each interval. In comparison to HTK, UW demonstrates a statistically significantly higher level of ATP after each interval of ischemia (p < 0.001) and reperfusion (p < 0.002). Additionally, UW-preserved human liver endothelial cells exceed the ATP level of the warm control during all intervals of ischemia. The loss of cell viability (LDH) was statistically significantly higher after ischemia (p < 0.01) and reperfusion (p < 0.01) in HTK than in UW except after the interval of 48 h. In conclusion, adenosine was more effective than α-ketoglutarate in maintaining a high ATP level in human liver endothelial cells after ischemia and reperfusion. Different pathways of energy substrate utilization were a contributing factor. The beneficial effect of the higher ATP level caused by adenosine to human liver endothelial cell viability was limited to 24 h of ischemia. Beyond this ischemia time we could not prove a favorable impact of adenosine on human liver endothelial cells.

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Experimental Liver Preservation with Celsior:A Novel Alternative to University of Wisconsin and Histidine-Tryptophan-α-Ketoglutarate Solutions?

Cited by 24 publications

References 25 publications

Celsior solution compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK) in the protection of human hepatocytes against ischemia-reperfusion injury

Celsior solution compared with University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK) in the protection of human hepatocytes against ischemia-reperfusion injury

A Natural Tetrahydropyrimidine Protects Small Bowel from Cold Ischemia and Subsequent Warm in vitro Reperfusion Injury

Value of Energy Substrates in HTK and UW to Protect Human Liver Endothelial Cells against Ischemia and Reperfusion Injury

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