Celsior solution (CS), a new preservation solution in thoracic organ transplantation, was evaluated for its efficacy in cold preservation of human liver endothelial cells (HLEC) and was compared to University of Wisconsin solution (UW) and histidine-tryptophan-ketoglutarate solution (HTK, Custodiol). HLEC cultures were preserved at 4°C in CS, UW, and HTK, for 2, 6, 12, 24, and 48 hours, with 6 hours of reperfusion. Levels of lactate dehydrogenase (LDH), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and adenosine 5-triphosphate (ATP) were measured after each interval of ischemia and the respective phase of reperfusion. Preservation injury of HLEC as measured by LDH release, intracellular ATP level, and MTT reduction were overall significantly (P < .01, P < .01, P < .05, respectively) lower in UW than in CS and HTK. CS demonstrates a modest superiority to HTK in HLEC preservation. Furthermore, cold preservation remains the main cause of preservation injury of HLEC regardless of the preservation solution used. Additionally, the maintenance of a high intracellular ATP level of HLEC after ischemia and reperfusion, as shown by UW, could be taken as a beneficial effect, particularly in long-term ischemia. In conclusion, our cell culture model reveals the order of efficacy to protect HLEC against preservation injury as: UW ӷ CS > HTK. (Liver
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.
We studied the course of serum bile acids to investigate its reliability in the diagnosis of acute rejection after liver transplantation in relation to pathohistological findings. Serum bile acid concentration, bilirubin and transaminases were measured in 41 patients who underwent liver transplantation. Their course was correlated to liver biopsy. Group I (n = 19) patients were without acute rejection, whereas group II (n = 22) patients showed acute rejection. Bile acid concentrations in group II showed a statistically highly significant (P < or = 0.001) threefold increase 3 days prior to biopsy. Successful antirejection treatment was correlated with a statistically significant (P = 0.008) decrease of serum bile acid 1 day after initiation of therapy. Patients without acute rejection showed a baseline bile acid concentration at the time of biopsy. Bilirubin and transaminases did not show any statistically significant correlation to acute rejection. Infection did not lead to a significant bile acid increase. Our study shows that serum bile acids monitored after liver transplantation can easily be used to detect acute rejection and at the same time they reflect the success of antirejection therapy.
We studied the course of serum bile acids to investigate its reliability in the diagnosis of acute rejection after liver transplantation in relation to pathohistological findings. Serum bile acid concentration, bilirubin and transaminases were measured in 41 patients who underwent liver transplantation. Their course was correlated to liver biopsy. Group I (n = 19) patients were without acute rejection, whereas group I1 (n = 22) patients showed acute rejection. Bile acid concentrations in group I1 showed a statistically highly significant ( P 2 0.001) threefold increase 3 days prior to biopsy. Successful antirejection treatment was correlated with a statistically significant ( P = 0.008) decrease of serum bile acid 1 day after initiation of therapy. Patients without acute rejection showed a baseline bile acid concentration at the time of biopsy. Bilirubin and transaminases did not show any statistically significant correlation to acute rejection.Infection did not lead to a significant bile acid increase. Our study shows that serum bile acids monitored after liver transplantation can easily be used to detect acute rejection and at the same time they reflect the success of antirejection therapy.
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