title: Glycohydrolases as markers of hepatic ischemia-reperfusion injury and recovery.
abstract: Advances in liver surgery and transplantation have lead to a steady increase in the number of these interventions. Prompt quantitative assessment of hepatic of hepatic function and a patient's subsequent morbidity and mortality following surgery remain difficult despite the currently utilized historic markers of hepatic parenchymal injury (e.g., aspartate transaminase [AST], lactate dehydrogenase [LDH] gamma-glutamyl transpeptidase [GGT]). Increases in serum glycohydrolase activities appear to provide sensitive and quantitative markers of hepatic ischemia/reperfusion injury. In 10 male swine (25 to 35 kg body weight) following 30, 45, and 90 minutes of acute hepatic ischemia, the systemic release of eight different glycohydrolases and lipid peroxides into serum were determined and compared with pre- and postischemic serum levels of LDH, GGT, and AST. The rapid release of glycohydrolases into serum was directly proportional to the length of the ischemic period from 30 to 90 minutes; e.g., beta-glucosidase, mean 1.9-fold increase at 30 minutes; 8.3-fold at 45 minutes; and 22.8-fold at 90 minutes; P < .002) and the activities peaked within the first 3 hours postischemia. In constrast, AST, LDH, and GGT were released slowly and peaked 20 to 30 hours after hepatic blood flow was restored. In swine with fatal outcomes (90 minutes of ischemia), all enzyme levels increased continuously during the final hours of life. However, in swine that survived hepatic ischemia/reperfusion injury (45 minutes of ischemia) the glycohydrolases, but not AST, LDH, and GGT, declined after 2 to 3 hours' postischemia and the serum lipid peroxide levels followed the same pattern. Serum beta-galactosidase and beta-glucosidase levels are sensitive markers that rise as quickly as traditional enzyme markers (AST, LDH, GGT) following hepatic ischemic injury; moreover, the glycohydrolases have the added value of serving as predictors of survival.
authors.affiliation: Department of Surgery, School of Medicine, University of New Mexico, Albuquerque, NM, USA..
authors.forename: W
authors.initials: W
authors.lastname: Liu
authors.forename: O
authors.initials: O
authors.lastname: Schöb
authors.forename: J E
authors.initials: JE
authors.lastname: Pugmire
authors.forename: D
authors.initials: D
authors.lastname: Jackson
authors.forename: K A
authors.initials: KA
authors.lastname: Zucker
authors.forename: D E
authors.initials: DE
authors.lastname: Fry
authors.forename: R H
authors.initials: RH
authors.lastname: Glew
mesh_terms: D000135:Acid Phosphatase / Q000032:analysis; D000818:Animals; D001011:Aorta; D015415:Biomarkers / Q000097:blood; D005966:Glucuronidase / Q000032:analysis; D006026:Glycoside Hydrolases / Q000032:analysis* / Q000097:blood; D006503:Hepatic Veins; D015227:Lipid Peroxidation; D008099:Liver / Q000098:blood supply* / Q000201:enzymology*; D008297:Male; D011169:Portal Vein; D015427:Reperfusion Injury; D013552:Swine; D013997:Time Factors; D000519:alpha-Galactosidase / Q000032:analysis; D000520:alpha-Glucosidases / Q000032:analysis; D001616:beta-Galactosidase / Q000032:analysis; D001617:beta-Glucosidase / Q000032:analysis; D001619:beta-N-Acetylhexosaminidases / Q000032:analysis
chemical_list: D015415:Biomarkers; D000135:Acid Phosphatase; D006026:Glycoside Hydrolases; D000520:alpha-Glucosidases; D001617:beta-Glucosidase; D000519:alpha-Galactosidase; D001616:beta-Galactosidase; D005966:Glucuronidase; D001619:beta-N-Acetylhexosaminidases