Abstract

Context Ischemia-reperfusion injury is a fascinating topic which has drawn a lot of interest in the last several years. Hepatic ischemia reperfusion injury may occur in a variety of clinical situations. These include transplantation, liver resection, trauma, and vascular surgery. Evidence Acquisition The purpose of this review was to outline the molecular mechanisms underlying hepatic I/R injury and present the latest approaches, both surgical and pharmacological, regarding the prevention of it. A comprehensive electronic literature search in MEDLINE/PubMed was performed to identify relative articles published within the last 2 years. Results The basic mechanism of hepatic ischemia – reperfusion injury is one of blood deprivation during ischemia, followed by the return of flow during reperfusion. It involves a complex series of events, such as mitochondrial deenergization, adenosine-5'-triphosphate depletion, alterations of electrolyte homeostasis, as well as Kupffer cell activation, oxidative stress changes and upregulation of proinflammatory cytokine signaling. The great number of variable pathways, with several mediators interacting with each other, leads to a high number of candidates for potential therapeutic intervention. As far as surgical approaches are concerned, the modification of existing clamping techniques and the ischemic preconditioning are the most promising techniques till recently. In the search for novel techniques of protecting against hepatic ischemia reperfusion injury, many different strategies have been used in experimental models. The biggest part of this research lies around antioxidant therapy, but other potential solutions have been explored as well. Conclusions The management of hepatic trauma, in spite of the fact that it has become increasingly nonoperative, there still remains the possibility of hepatic resection in the hepatic trauma setting, especially in severe injuries. Hence, clinicians should be familiar with the concept of hepatic ischemia-reperfusion injury and respond appropriately and timely.

Highlights

  • Context: Ischemia-reperfusion injury is a fascinating topic which has drawn a lot of interest in the last several years

  • In the search for novel techniques of protecting against hepatic ischemia reperfusion injury, many different strategies have been used in experimental models

  • Activation of Kupffer cells (KC) with production of reactive oxygen species (ROS), upregulation of the inducible nitric oxide synthase in hepatocytes, and upregulation of proinflammatory cytokines, chemokines, and adhesion molecules resulting in neutrophil-mediated injury, are all major contributing events to the inflammation-associated damage [13]

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Summary

Introduction

Context: Ischemia-reperfusion injury is a fascinating topic which has drawn a lot of interest in the last several years. Hepatic ischemia reperfusion injury may occur in a variety of clinical situations These include transplantation, liver resection, trauma, and vascular surgery. Results: The basic mechanism of hepatic ischemia – reperfusion injury is one of blood deprivation during ischemia, followed by the return of flow during reperfusion It involves a complex series of events, such as mitochondrial deenergization, adenosine-5'-triphosphate depletion, alterations of electrolyte homeostasis, as well as Kupffer cell activation, oxidative stress changes and upregulation of proinflammatory cytokine signaling. Ischemia reperfusion injury (IRI) is defined as the phenomenon during which cellular damage in an organ, caused by hypoxia, is paradoxically exacerbated after the restoration of oxygen delivery [1] It is a dynamic process which involves the two interrelated phases of local ischemic insult and inflammation-mediated reperfusion injury [2]. Warm ischemia occurs in the setting of transplantation, trauma, shock, and elective liver surgery, in which hepatic blood supply is temporarily interrupted. Emphasis was given on identifying the most recent data on the mechanisms involved in hepatic ischemia/reperfusion injury

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