Graft reconditioning with nitric oxide gas in rat liver transplantation from cardiac death donors

Transplantation. 2014 Mar 27;97(6):618-25. doi: 10.1097/TP.0000000000000025.

Abstract

Background: Liver transplant outcomes using grafts donated after cardiac death (DCD) remain poor.

Methods: We investigated the effects of ex vivo reconditioning of DCD grafts with venous systemic oxygen persufflation using nitric oxide gas (VSOP-NO) in rat liver transplants. Orthotopic liver transplants were performed in Lewis rats, using DCD grafts prepared using static cold storage alone (group-control) or reconditioning using VSOP-NO during cold storage (group-VSOP-NO). Experiment I: In a 30-min warm ischemia model, graft damage and hepatic expression of inflammatory cytokines, endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and endothelin-1 (ET-1) were examined, and histologic analysis was performed 2, 6, 24, and 72 hr after transplantation. Experiment II: In a 60-min warm ischemia model, grafts were evaluated 2 hr after transplantation (6 rats/group), and survival was assessed (7 rats/group).

Results: Experiment I: Group-VSOP-NO had lower alanine aminotransferase (ALT) (P<0.001), hyaluronic acid (P<0.05), and malondialdehyde (MDA) (P<0.001), hepatic interleukin-6 expression (IL-6) (P<0.05), and hepatic tumor necrosis factor-alpha (TNF-α) expression (P<0.001). Hepatic eNOS expression (P<0.001) was upregulated, whereas hepatic iNOS (P<0.01) and ET-1 (P<0.001) expressions were downregulated. The damage of hepatocyte and sinusoidal endothelial cells (SECs) were lower in group-VSOP-NO.Experiment II: VSOP-NO decreased ET-1 and 8-hydroxy-2'deoxyguanosine (8-OHdG) expression and improved survival after transplantation by 71.4% (P<0.01).

Conclusion: These results suggest that VSOP-NO effectively reconditions warm ischemia-damaged grafts, presumably by decreasing ET-1 upregulation and oxidative damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 8-Hydroxy-2'-Deoxyguanosine
  • Alanine Transaminase / metabolism
  • Animals
  • Cold Ischemia
  • Cytokines / genetics
  • Cytokines / metabolism
  • Cytoprotection
  • Deoxyguanosine / analogs & derivatives
  • Deoxyguanosine / metabolism
  • Endothelin-1 / genetics
  • Endothelin-1 / metabolism
  • Gases
  • Hyaluronic Acid / metabolism
  • Inflammation Mediators / metabolism
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Liver / surgery*
  • Liver Transplantation / adverse effects*
  • Malondialdehyde / metabolism
  • Models, Animal
  • Nitric Oxide / pharmacology*
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred Lew
  • Reperfusion Injury / etiology
  • Reperfusion Injury / genetics
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / pathology
  • Reperfusion Injury / prevention & control*
  • Time Factors
  • Warm Ischemia / adverse effects

Substances

  • Cytokines
  • Endothelin-1
  • Gases
  • Inflammation Mediators
  • RNA, Messenger
  • Nitric Oxide
  • Malondialdehyde
  • 8-Hydroxy-2'-Deoxyguanosine
  • Hyaluronic Acid
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Nos2 protein, rat
  • Nos3 protein, rat
  • Alanine Transaminase
  • Deoxyguanosine