title: Glycolytic support of adenine nucleotides in rat liver flush-preserved with UW or Collins' II. Importance of donor nutritional status.
abstract: Correlation of hepatocellular adenine nucleotides in donor liver with clinical posttransplant outcome has recently been reported. Our earlier work with rats has shown that pretreatment of donors with glucose effectively retards hepatocellular ATP losses in livers preserved in Collins' II solution through potentiation of their glycolytic capacity. The primary substrate--i.e., endogenous or exogenous glucose--was not identified. The current study was undertaken to compare the relative efficacy of the University of Wisconsin (UW) solution, which is devoid of glucose, with Collins' II in the support of adenine nucleotides through anaerobic glycolysis in flush-preserved rat liver. Adult rats were either pretreated with 25% dextrose or fasted prior to liver harvesting and preservation in either UW or Collins' II. Adenine nucleotide degradation and lactate production during preservation were assessed. For a given dietary pretreatment, losses of ATP and adenylate energy charge and lactate production were similar for UW- and Collins' II-preserved livers. Donor pretreatment with dextrose resulted in significantly higher ex vivo liver ATP, energy charge, and lactate regardless of the preservation solution. Salvageable nucleotide degradates were increased significantly in UW livers, presumably through the effects of allopurinol. These results demonstrate that effective support of adenine nucleotides by glycolysis in flush-preserved liver is independent of the presence of exogenous glucose but dependent upon the nutritional status of the donor prior to liver procurement.
authors.affiliation: Laboratory of Nutrition and Infection, New England Deaconess Hospital/Harvard Medical School, Boston, Massachusetts 02215.
authors.forename: J D
authors.initials: JD
authors.lastname: Palombo
authors.forename: J J
authors.initials: JJ
authors.lastname: Pomposelli
authors.forename: Y
authors.initials: Y
authors.lastname: Hirschberg
authors.forename: G L
authors.initials: GL
authors.lastname: Blackburn
authors.forename: B R
authors.initials: BR
authors.lastname: Bistrian
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism*; D000241:Adenosine; D000493:Allopurinol; D000818:Animals; D005978:Glutathione; D006019:Glycolysis; D006982:Hypertonic Solutions / Q000494:pharmacology*; D007328:Insulin; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008099:Liver / Q000378:metabolism; D016031:Liver Transplantation; D008297:Male; D009752:Nutritional Status; D009926:Organ Preservation / Q000379:methods*; D019188:Organ Preservation Solutions; D009929:Organ Size; D011887:Raffinose; D051381:Rats; D011919:Rats, Inbred Strains; D012996:Solutions / Q000494:pharmacology*
chemical_list: D000227:Adenine Nucleotides; C024102:Collins' solution; D006982:Hypertonic Solutions; D007328:Insulin; D007773:Lactates; D019188:Organ Preservation Solutions; D012996:Solutions; C055206:University of Wisconsin-lactobionate solution; D019344:Lactic Acid; D000493:Allopurinol; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose