Mechanism and prevention of ischemia-reperfusion injury of the liver

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Abstract
Interruption of liver blood flow is often necessary as an operative technique in liver surgery. However, this procedure causes liver damage and can be a factor in postoperative liver failure. Interruption of oxygen and substrate supply and accumulation of metabolites contribute to a great variety of cellular and subcellular dysfunctions. Impairment of liver microcirculation occurs after reperfusion. It has been presumed that there is an imbalance between the activities of vasoconstrictors and vasodilators which would determine the vascular condition during ischemia and reperfusion phases. Some mediators are known to act as cytotoxic factors, especially after reperfusion following ischemia. The phenomenon in which organ damage becomes worse, even after reperfusion, is called reperfusion injury. Mediators released from accumulated polymorphonuclear neutrophils and activated Kupffer cells such as oxygen radicals and inflammatory cytokines are associated with ischemia‐reperfusion injury of the liver. Regulation of these mediators will be a therapeutic necessity for this kind of liver injury in the future.