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Changes in Energy Metabolism of Allografts after Liver Transplantation

 

作者: T. Morimoto,   M. Ukikusa,   Y. Taki,   K. Koizumi,   N. Yokoo,   A. Tanaka,   M. Noguchi,   S. Yamamoto,   N. Nitta,   Y. Kamiyama,   Y. Yamaoka,   K. Ozawa,  

 

期刊: European Surgical Research  (Karger Available online 1988)
卷期: Volume 20, issue 2  

页码: 120-127

 

ISSN:0014-312X

 

年代: 1988

 

DOI:10.1159/000128750

 

出版商: S. Karger AG

 

关键词: Liver transplantation;Liver mitochondria;Respiratory components;Hepatic energy charge;Oxidative phosphorylative activity;Arterial blood ketone body ratio;Mitochondrial oxidoreduction state (redox state)

 

数据来源: Karger

 

摘要:

To evaluate the function of energy metabolism in allografts after liver transplantation, changes in hepatic energy charge levels, oxidative and phosphorylative activities of mitochondria and arterial blood ketone body ratio (acetoacetate/3-hydroxybutyrate; KBR) were studied in piglets. Hepatic energy charge levels decreased to 0.831 ± 0.010 at 3 days and 0.836 ± 0.009 at 3 weeks after operation compared to the preoperative value of 0.868 ± 0.006 (p < 0.01), and returned to 0.856 ± 0.007 at 6 weeks. Mitochondrial oxidative and phosphorylative activities were moderately enhanced to 19.14 ± 2.07 (10–10 mol ATP/mg of mitochondrial protein/s) at 3 days and 20.89 ± 1.72 at 3 weeks compared to the preoperative value of 16.74 ± 2.36, and returned to 16.65 ± 1.54 at 6 weeks. There was no significant difference in the concentrations of mitochondrial respiratory components, except in cytochrome c + c1. KBR decreased immediately at the beginning of the anhepatic phase and rapidly recovered to the preoperative level within 60 min after revascularization of allografts. There was no change in KBR during the postoperative course except in cases with clinical deterioration. From these results, it is suggested that the mitochondrial capacity for ATP synthesis was enhanced to compensate for the decreased energy charge level and that a decreased KBR is a sign of a critically deranged metabolic function in a

 

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