Hepatic ischemia-reperfusion injury in liver transplant setting: mechanisms and protective strategies.

Ding Ma ,Sanketh Rampes

doi:10.7555/jbr.32.20180087

Ding Ma , Sanketh Rampes

Open Access

https://doi.org/10.7555/jbr.32.20180087

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Journal: Journal of biomedical research	Publication Date: Jan 1, 2019
Citations: 64	License type: cc-by

Affiliation: King's College London

Abstract

Hepatic ischemia-reperfusion injury is a major cause of liver transplant failure, and is of increasing significance due to increased use of expanded criteria livers for transplantation. This review summarizes the mechanisms and protective strategies for hepatic ischemia-reperfusion injury in the context of liver transplantation. Pharmacological therapies, the use of pre-and post-conditioning and machine perfusion are discussed as protective strategies. The use of machine perfusion offers significant potential in the reconditioning of liver grafts and the prevention of hepatic ischemia-reperfusion injury, and is an exciting and active area of research, which needs more study clinically.

Highlights

Hepatic ischemia-reperfusion injury (IRI) is a pathological process that involves ischemia-mediated cellular damage followed by a paradoxical exacerbation upon reperfusion of the liver
The first clinical study of normothermic machine perfusion (NMP) in 16 donors after brain death (DBD) livers and 4 donors after cardiac death (DCD) livers showed significantly lower peak aspartate transaminase (AST) in the first week postoperatively compared to static cold storage (SCS) controls, which may indicate a reduction in the severity of hepatic IRI[146]
Hepatic IRI is a pathological process, which involves ischemia-mediated cellular damage exacerbated upon reperfusion

Summary

Introduction

Hepatic ischemia-reperfusion injury (IRI) is a pathological process that involves ischemia-mediated cellular damage followed by a paradoxical exacerbation upon reperfusion of the liver. The key processes and factors involved in hepatic IRI are: oxidative stress, anaerobic metabolism, nitrous oxide (NO), KCs and neutrophils, mitochondria, intracellular calcium overload, cytokines and chemokines (Fig. 2). Endothelial NOS (eNOS) has been shown to be protective in hepatic IRI through counteracting the deleterious effects of ROS on the liver[55]. Reperfusion of the ischemic liver triggers the release of cytokines responsible for initiating and maintaining an inflammatory response, which causes hepatic IRI[70].

Results

Conclusion