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Review
. 2015;2(1):52-62.
doi: 10.1007/s40472-014-0046-1.

Hypothermic Oxygenated Liver Perfusion: Basic Mechanisms and Clinical Application

A Schlegel  1 , P Kron  1 , P Dutkowski  1
Affiliations
Review

Hypothermic Oxygenated Liver Perfusion: Basic Mechanisms and Clinical Application

A Schlegel et al. Curr Transplant Rep. 2015.

Abstract

Dynamic preservation strategies such as hypothermic machine perfusion are increasingly discussed to improve liver graft quality before transplantation. This review summarizes current knowledge of this perfusion technique for liver preservation. We discuss optimization of perfusion conditions and current strategies to assess graft quality during cold perfusion. Next, we provide an overview of possible pathways of protection from ischemia-reperfusion injury. Finally, we report on recent clinical applications of human hypothermic machine liver perfusion.

Keywords: Hypothermic oxygenated perfusion; Ischemia-reperfusion injury; Mitochondria; ROS.

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Figures

Fig. 1
Fig. 1
Perfusion flow at low pressure (3 mmHg) appears comparable for different species (rat, pig, human), if related to liver weight (A, B). Oxygen consumption during hypothermic machine liver perfusion decreases during the first hour of perfusion and stays at a low level during further perfusion (C). Angiography during low-pressure hypothermic perfusion of pig DCD livers demonstrates complete perfusion of all sinusoids within the first minutes by exclusively portal vein perfusion (D)
Fig. 2
Fig. 2
Physiological release of reactive oxygen species (ROS) occurs in mitochondria between complex II and III. During ischemia reperfusion, however, this ROS release increases significantly and can initiate opening of the mitochondrial permeability transition pore complex (MPT-pore). Subsequently, mitochondrial proteins (cytochrome C, Smac/DIABLO, endonuclease G, AIF) are released in the cytosol, which activate different cell organelles. Hypothermic oxygenated perfusion prevents the initial mitochondrial ROS release
Fig. 3
Fig. 3
ROS release from mitochondria leads to nuclear injury and release of danger-associated molecular patterns (DAMPs) (A), which in turn stimulate Kupffer cells via Toll-like receptors once released by hepatocytes (B). Activated Kupffer cells release mediators and intravasal ROS (C), which activate downstream endothelial cells and platelets (D)
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