title: Ischemic injury in cirrhotic livers: an experimental study of the temporary arrest of hepatic circulation.
abstract: In order to prevent massive bleeding at hepatectomy, the temporary arrest of hepatic circulation is often performed but it is not clear whether this arrest of circulation is tolerated equally by the cirrhotic liver and the normal liver. We investigated biochemically the detailed effects of ischemia on cirrhotic livers in rats with experimentally induced liver cirrhosis. Thioacetoamide was used to prepare the rat cirrhotic liver model (LC group, n = 6). After laparotomy, the vessels to the left lateral lobe were clamped for 30 min and then declamped. Changes in AST isozymes and the aminogram in the blood were examined after ischemia. Postischemic changes in hepatic adenine nucleotides (AdN) and the brain aminogram were also examined. These were compared with those of normal liver ischemia (N group, n = 6) at 24 hr after recirculation. In the LC group, serum levels of mitochondrial AST, a parameter of necrotic cells, were significantly higher than those of the N group. Hepatic AdN levels decreased to 60.6% of the original levels after ischemic injury but those of the N group remained at 95.4% of the original level. Since AdN in tissue is accepted as a reliable parameter of viable cells, cirrhotic livers subjected to ischemia might have more necrotic cells than normal livers. Sequential analysis of serum aminograms of the LC group after ischemia revealed that the ratio of Val+Leu+Ileu/Tyr+Phe decreased to near 1.0 but that of the N group always remained higher than 3.0. Based on these results, it was concluded that ischemic injury in cirrhotic livers is more hazardous than that in normal livers.
authors.affiliation: Department of Surgery, Kure National Hospital, Hiroshima, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Nishimura
authors.forename: M
authors.initials: M
authors.lastname: Nakahara
authors.forename: S
authors.initials: S
authors.lastname: Kobayashi
authors.forename: I
authors.initials: I
authors.lastname: Hotta
authors.forename: S
authors.initials: S
authors.lastname: Yamawaki
authors.forename: Y
authors.initials: Y
authors.lastname: Marui
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000596:Amino Acids / Q000097:blood / Q000378:metabolism; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001921:Brain / Q000378:metabolism; D004569:Electroencephalography; D004734:Energy Metabolism; D007511:Ischemia; D007527:Isoenzymes / Q000097:blood; D008099:Liver / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000473:pathology / Q000601:surgery*; D008297:Male; D009043:Motor Activity; D051381:Rats; D015427:Reperfusion Injury / Q000503:physiopathology; D013853:Thioacetamide
chemical_list: D000596:Amino Acids; D007527:Isoenzymes; D013853:Thioacetamide; D000255:Adenosine Triphosphate; D001219:Aspartate Aminotransferases