Adrenaline and Dopamine in Porcine Livers After Cold Preservation With University of Wisconsin Histidine-Tryptophan-Ketoglutarate, Prolactin-Modified Histidine-Tryptophan-Ketoglutarate Solutions

作者:Budzinski G*; Suszka Switek A; Dec R; Caban A; Wystrychowski W; Oczkowicz G; Heitzman M; Dolinska B; Ryszka F; Cierpka L
来源:Transplantation Proceedings, 2011, 43(8): 2895-2896.
DOI:10.1016/j.transproceed.2011.08.063

摘要

Introduction. Hepatic ischemia-reperfusion injury remains a significant factor influencing early liver graft function. The aim of this study was to assess the impact on hepatic ischemia as reflected by catecholarnine concentrations of different methods of organ preservation.
Materials and methods. Catecholamine levels were measured in 24 (n = 6/group) pig livers, which underwent 30-minute warm ischemia followed by 30-minute perfusion and subsequent cold storage for 12 hours. For perfusion and preservation, we used University of Wisconsin (UW), histidine-tryptophan-ketoglutarate (HTK), HTK-modified with prolactin (PRL) or Ringer's solutions. Dopamine (DO) and adrenaline (ADR) concentrations in liver venous effluents were assayed using a radioimmunological method after 30 minutes of perfusion and following 12 hours of preservation.
Results. DO and ADR levels were higher after 12 hours preservation compared to 30 minutes of perfusion. HTK produced an increase of over 100%. Addition of PRL (20 IU/L) did not affect DO and ADR levels after 30 minutes of perfusion, but significantly decreased their concentrations at 12 hours of preservation. After UW perfusion and preservation, we observed a 10% increase in catecholamine levels as compared with postperfusion values. Preservation with Ringer's solution demonstrated significantly higher DO and ADR levels compared with other solutions.
Conclusion. Catecholamines are present in the liver after 30 minute of perfusion and 12 hours of cold storage. The increased levels after 12 hours of preservation may be due to their release from intracellular spaces (as a controlled process or as a result of necrosis). It may play a crucial role in reperfusion injury, which, in turn, may explain the mechanism of no-reflow phenomenon.

  • 出版日期2011-10

全文