Abstract
We describe in this review the different types of injuries caused to the biliary tree after liver transplantation. Furthermore, we explain underlying mechanisms and why oxygenated perfusion concepts could not only protect livers, but also repair high-risk grafts to prevent severe biliary complications and graft loss. Accordingly, we summarize experimental studies and clinical applications of machine liver perfusion with a focus on biliary complications after liver transplantation. Key points: (1) Acute inflammation with subsequent chronic ongoing liver inflammation and injury are the main triggers for cholangiocyte injury and biliary tree transformation, including non-anastomotic strictures; (2) Hypothermic oxygenated perfusion (HOPE) protects livers from initial oxidative injury at normothermic reperfusion after liver transplantation. This is a unique feature of a cold oxygenation approach, which is effective also end-ischemically, e.g., after cold storage, due to mitochondrial repair mechanisms. In contrast, normothermic oxygenated perfusion concepts protect by reducing cold ischemia, and are therefore most beneficial when applied instead of cold storage; (3) Due to less downstream activation of cholangiocytes, hypothermic oxygenated perfusion also significantly reduces the development of biliary strictures after liver transplantation.
Highlights
The ultimate goal and task for new preservation strategies is to treat and repair high-risk organs, which were previously deemed not transplantable
The major problems in the field remain the biliary complications after liver transplantation, and there are two main strategies physicians put their focus on [2]
The second is to treat livers before implantation to improve their quality with the use of novel machine perfusion technology [4]
Summary
The ultimate goal and task for new preservation strategies is to treat and repair high-risk organs, which were previously deemed not transplantable. Short periods of ischemia already induce a rapid cellular energy depletion in the very sensitive biliary epithelial cells (cholangiocytes) [9], which subsequently detach from the basement membrane due to a loss of their intercellular connections In this context, several clinical studies have described a significant loss of epithelial cells in large extrahepatic bile ducts after transplantation of otherwise relatively low-risk livers, donated after brain death (DBD) [10]. The current main explanation for a higher rate of NAS in DCD transplants is an initial cellular lack of oxygen in hepatocytes and cholangiocytes, leading first to insufficient oxygenation of the progenitor niche with subsequently impaired regeneration of the larger bile ducts [11].
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