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, 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 degrees 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; mitochondrial 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.
Janssen
Hermann
H
Klinik für Allgemein- und Thoraxchirurgie, Justus-Liebig-Universität Giessen, Rudolf-Buchheim-Strasse 7, 35385, Giessen, Germany. hermann.janszen@t-online.de
Janssen
Petra H E
PH
Broelsch
Christoph E
CE
D000241:Adenosine / Q000494:pharmacology*; D000255:Adenosine Triphosphate / Q000378:metabolism; D000493:Allopurinol / Q000494:pharmacology*; D002478:Cells, Cultured; D015925:Cryopreservation; D004187:Disaccharides / Q000494:pharmacology*; D004573:Electrolytes / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology*; D005971:Glutamates / Q000494:pharmacology*; D005978:Glutathione / Q000494:pharmacology*; D022781:Hepatocytes / Q000187:drug effects* / Q000378:metabolism; D006639:Histidine / Q000494:pharmacology*; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008353:Mannitol / Q000494:pharmacology*; D019188:Organ Preservation Solutions / Q000494:pharmacology*; D010084:Oxidation-Reduction / Q000187:drug effects; D011189:Potassium Chloride / Q000494:pharmacology*; D011343:Procaine / Q000494:pharmacology*; D011887:Raffinose / Q000494:pharmacology*; D015427:Reperfusion Injury / Q000517:prevention & control*; D013778:Tetrazolium Salts / Q000378:metabolism; D013844:Thiazoles / Q000378:metabolism
C039984:Bretschneider cardioplegic solution; C088453:Celsior; D004187:Disaccharides; D004573:Electrolytes; D005971:Glutamates; D007328:Insulin; D019188:Organ Preservation Solutions; D013778:Tetrazolium Salts; D013844:Thiazoles; C055206:University of Wisconsin-lactobionate solution; D008353:Mannitol; D006639:Histidine; D011343:Procaine; D000493:Allopurinol; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; C022616:thiazolyl blue; D005978:Glutathione; D005947:Glucose; D000241:Adenosine; D011887:Raffinose