ism itself. A number of hypotheses have been articulated to Advances in liver surgery and transplantation have provide mechanistic explanations for reperfusion injury: free lead to a steady increase in the number of these interradical generation and attack of unsaturated lipids, proteins, ventions. Prompt quantitative assessment of hepatic and nucleic acids; increased turnover of membrane phosphofunction and a patient's subsequent morbidity and morlipids; and disturbances of calcium homeostasis at the cellutality following surgery remain difficult despite the curlar level. The liver is one of the organs that is most sensitive to hepatic ischemia, the systemic release of eight different ischemia. [5][6][7] Advances in liver surgery and liver transplantaglycohydrolases and lipid peroxides into serum were de-tion in particular have stimulated the search for quantitative termined and compared with pre-and postischemic se-biochemical markers that would provide surgeons and clinirum levels of LDH, GGT, and AST. The rapid release of cians with a means of assessing objectively and expeditiously glycohydrolases into serum was directly proportional to the functional integrity of the liver after various surgeries the length of the ischemic period from 30 to 90 minutes have been performed, in particular those which require iso-(e.g., b-glucosidase, mean 1.9-fold increase at 30 minutes; lating the organ from its normal blood supply for significant 8.3-fold at 45 minutes; and 22.8-fold at 90 minutes; P õ periods of time. The enzymes that have been used historically .002) and the activities peaked within the first 3 hours' and which are still relied upon today to monitor liver function postischemia. In contrast, AST, LDH, and GGT were re-postsurgically, include lactate dehydrogenase (LDH), g-gluleased slowly and peaked 20 to 30 hours after hepatic tamyl transpeptidase (GGT), and aspartate transaminase blood flow was restored. In swine with fatal outcomes (AST). Increased plasma activities of a number of glycohydro-(90 minutes of ischemia), all enzyme levels increased lases have been found to result from a variety of liver injuries, continuously during the final hours of life. However, in including: carbon tetrachloride-induced liver cirrhosis, 8 parswine that survived hepatic ischemia/reperfusion injury tial hepatectomy, 9,10 hepatic dearterialization, 11 hepatic cryo-(45 minutes of ischemia) the glycohydrolases, but not surgery, 12 and cold and warm hepatic ischemia. [13][14][15] Free radi-AST, LDH, and GGT, declined after 2 to 3 hours' postisch-cals produced by liver injury are thought to be the mediators emia and the serum lipid peroxide levels followed the responsible for hepatic damage and have been described in same pattern. Serum b-galactosidase and b-glucosidase many animal models. 6,7,16-18 In 1991, Chang et al. 19 reported levels are sensitive markers that rise as quickly as tradi-that following liver transplantation in the pig the activity tional enzyme markers (AST, LDH, GGT) following he-levels of several glycohy...
