title: Heat shock preconditioning ameliorates liver injury following normothermic ischemia-reperfusion in steatotic rat livers.
abstract: The decreased tolerance of steatotic livers to warm ischemia complicates liver surgery. The efficacy of heat shock preconditioning in steatotic livers to lessen ischemia-reperfusion injury was studied in rats. Steatotic liver was produced in Lewis rats with a choline-deficient diet. Rats with steatotic livers were divided into a heat shock preconditioned group (group HS) and a control group (group C). All rats received 45 min of hepatic warm ischemia. Survival rates and changes in biochemical and histological parameters were compared in both groups. Heat shock protein 72 (HSP72) was produced only in group HS. The 7-day survival of the rats after warm ischemic intervention was significantly better in group HS (13/15) than in group C (5/15) (P < 0.01). The concentration of ATP in liver tissue (n = 10, P < 0.01) and serum levels of aspartate aminotransferase (n = 10, P < 0.05), alanine aminotransferase (n = 10, P < 0.01), and lactic dehydrogenase (n = 10, P < 0.01) at 40 min reperfusion were also significantly better in group HS than in group C. Histological examination at 40 min reperfusion showed severe sinusoidal congestion, hepatocyte necrosis, and increased positivity to 4-hydroxy-2-nonenal-modified proteins in group C livers; these signs were markedly suppressed in group HS livers. The data indicate that heat shock preconditioning provides the steatotic rat liver with significant tolerance to warm ischemia-reperfusion injury.
authors.affiliation: Department of Gastroenterological Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yamagami
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: M
authors.initials: M
authors.lastname: Kume
authors.forename: S
authors.initials: S
authors.lastname: Kimoto
authors.forename: H
authors.initials: H
authors.lastname: Yamamoto
authors.forename: N
authors.initials: N
authors.lastname: Ozaki
authors.forename: M
authors.initials: M
authors.lastname: Yamamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Shimahara
authors.forename: S
authors.initials: S
authors.lastname: Toyokuni
authors.forename: Y
authors.initials: Y
authors.lastname: Yamaoka
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D005234:Fatty Liver / Q000473:pathology / Q000503:physiopathology*; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006358:Hot Temperature; D019194:Ischemic Preconditioning; D015227:Lipid Peroxidation; D008099:Liver / Q000098:blood supply* / Q000473:pathology; D008297:Male; D051381:Rats; D011917:Rats, Inbred Lew; D015427:Reperfusion Injury / Q000517:prevention & control*
chemical_list: D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D000255:Adenosine Triphosphate; D001219:Aspartate Aminotransferases