Changes in mitochondrial respiratory enzyme activity after ischemia-reperfusion injury in living-donor liver transplantation

Transplant Proc. 2010 Apr;42(3):721-4. doi: 10.1016/j.transproceed.2010.03.008.

Abstract

Background: Ischemia-reperfusion (I-R) injury plays an important role in the immediate graft function in living-donor liver transplantation (LDLT). There is growing evidence that mitochondria play a pivotal role in I-R injury. Our aim was to evaluate changes in mitochondrial respiratory enzyme activities after I-R injury in LDLT.

Methods: Specimens from 8 donor recipient pairs enrolled in this study were obtained from the donor livers before harvest (before I-R injury) and after vascular anastomosis in the recipient (after I-R injury). Histidine-tryptophan-ketoglutarate solution was used to perfuse the organ during the cold ischemic period between harvesting and transplantation. We correlated changes in mitochondrial respiratory enzyme complex activity (succinate cytochrome c reductase [SCCR]; NADH cytochrome c reductase [NCCR]) after I-R injury with clinical data and graft status.

Results: NCCR and SCCR activities did not uniformly decrease after I-R injury. Two of 8 recipients experienced graft dysfunction after transplantation. The decrease in neither NCCR nor SCCR activity correlated with graft dysfunction in these 2 patients. Among the clinical factors, grafts from older donors tended to show decreased NCCR activity after I-R injury.

Conclusions: In this study, changes in mitochondrial respiratory enzyme activity failed to predict the severity of I-R injury in LDLT. The organ preservation solution may play a protective role on mitochondrial respiratory enzymes during I-R injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Age Factors
  • Aged
  • Biomarkers
  • Female
  • Humans
  • Kinetics
  • Liver Transplantation / adverse effects*
  • Living Donors*
  • Male
  • Middle Aged
  • Mitochondria, Liver / enzymology*
  • NADH Dehydrogenase / metabolism*
  • Reperfusion Injury / enzymology*
  • Succinate Cytochrome c Oxidoreductase / metabolism*
  • Treatment Failure
  • Treatment Outcome

Substances

  • Biomarkers
  • Succinate Cytochrome c Oxidoreductase
  • NADH Dehydrogenase