Mechanism of Hepatic Ischemia/Reperfusion Injury and Protection Against Reperfusion Injury

Abstract

THE ISCHEMIA/REPERFUSION injury remains a problem after liver surgery or liver transplantation. Preservation injury is a major cause of primary nonfunction following liver transplantation. Sinusoidal endothelial cell (SEC) apoptosis is an outcome of cold ischemia/reperfusion injury. Investigators demonstrated a selective induction of apoptosis in sinusoidal and vascular endothelial cells within the liver following cold ischemia/warm reperfusion injury. Recent data also have indicated that platelet and leukocyte adhesion to the sinusoids mediate reperfusion injury by causing endothelial cell apoptosis. Ischemic precondition- ing, namely, a short period of ischemia prior to a major ischemic insult, is highly protective to downregulate the caspase pathway and inhibit apoptotic cell death.¹,² Future research on ischemic livers should focus on mechanisms and mediators involved in apoptotic cell death, which may lead to innovative protective strategies and preservation solutions with important clinical implications.