Published online Jan 27, 2014. doi: 10.4254/wjh.v6.i1.1
Revised: December 2, 2013
Accepted: December 17, 2013
Published online: January 27, 2014
Ischemia-reperfusion plays a major role in the injury experienced by the liver during transplantation. Much work has been done recently investigating the role of redox species in hepatic ischemia-reperfusion. As animal models are better characterized and developed, and more insights are gained into the pathophysiology of hepatic ischemia reperfusion injury in humans the questions into exactly how oxidants participate in this injury are becoming more refined. These questions include effects of cellular location, timing of injury, and ability of therapeutics to access this site are increasing our appreciation of the complexity of ischemia reperfusion and improving attempts to ameliorate its effects. In this review, we aim to discuss the various methods to alter redox chemistry during ischemia reperfusion injury and future prospects for preventing organ injury during hepatic ischemia reperfusion.
Core tip: Reactive oxygen and nitrogen species play a central role in the pathology of ischemia-reperfusion injury. In this review we discuss the efforts of many groups to trial therapeutics to ameliorate this damage in animal models of disease as well as clinical trials in humans. The failure of some trials has served to highlight the complexity of timing and compartmentalization of Ischemia Reperfusion injury. Finally, we discuss the emerging potential of replenishing nitric oxide by nitrite therapy and the uniquely broad therapeutic profile of nitrite.