Janssen Hermann, Janssen Petra H E, Broelsch Christoph E
Klinik für Allgemein- und Transplantationschirurgie, Universitätsklinikum Essen, Essen, Germany.
Eur Surg Res. 2004 Jan-Feb;36(1):26-32. doi: 10.1159/000075071.
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; alpha-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 degrees 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 alpha-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.
在器官移植的缺血和再灌注过程中，三磷酸腺苷（ATP）耗竭是细胞损伤的主要原因。因此，组氨酸 - 色氨酸 - 酮戊二酸溶液（HTK；α - 酮戊二酸）和威斯康星大学溶液（UW；腺苷）被提供能量底物以实现移植物的存活能力。然而，它们维持ATP水平的功效，尤其是在人肝内皮细胞中，尚不确定。此外，高ATP水平对人肝内皮细胞活力是否有益也备受关注。我们在细胞培养模型中使用第3至6代的人肝内皮细胞。将人肝内皮细胞在HTK和UW中于低温（4℃）下保存2、6、12、24和48小时，随后再灌注6小时。在每个时间间隔后测量ATP和乳酸脱氢酶（LDH）。与HTK相比，UW在缺血（p < 0.001）和再灌注（p < 0.002）的每个时间间隔后均显示出统计学上显著更高的ATP水平。此外，在所有缺血时间间隔内，UW保存的人肝内皮细胞的ATP水平超过了温育对照。除48小时时间间隔外，HTK组在缺血（p < 0.01）和再灌注（p < 0.01）后细胞活力丧失（LDH）在统计学上显著高于UW组。总之，在缺血和再灌注后人肝内皮细胞中，腺苷在维持高ATP水平方面比α - 酮戊二酸更有效。能量底物利用的不同途径是一个促成因素。腺苷导致的较高ATP水平对人肝内皮细胞活力的有益作用仅限于24小时缺血。超过这个缺血时间，我们无法证明腺苷对人肝内皮细胞有有利影响。
