Mechanism of Hepatic Ischemia/Reperfusion Injury and Protection Against Reperfusion Injury
- K.J. Kang
- Publication Year
- 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
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.
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