ABSTRACT
In hypoxic liver injury, the underlying circulatory problem is often the focus of attention rather than the liver itself. Hypoxia initiates a characteristic progression of structural changes in liver, heart, and other tissues. Bleb formation also occurs during anoxia and chemical hypoxia in isolated hepatocytes. Shedding of blebs apparently accounts for enzyme release by damaged livers in the absence of outright hepatic necrosis. Oxygen free radicals appear to be involved in lethal midzonal injury during low flow as follows: As low-flow hypoxia produces anoxia in pericentral zones of the liver lobule, adenosine triphosphate decreases, and hypoxanthine accumulates. Reperfusion injury in isolated perfused rat livers is more pronounced in the low-flow, reflow model of liver hypoxia. Extrinsic mechanisms involving blood-borne neutrophils also play a role in hepatic reperfusion injury. Rearterialization could influence surgical outcome since hypoxic and reperfusion injury to parenchymal as well as bile duct cells is triggered by limited oxygen availability.
