The role of bile salt toxicity in the pathogenesis of bile duct injury after non-heart-beating porcine liver transplantation

Transplantation. 2008 Jun 15;85(11):1625-31. doi: 10.1097/TP.0b013e318170f5f7.

Abstract

Background: Intrahepatic bile duct strictures are a serious complication after non-heart-beating (NHB) liver transplantation. Bile salt toxicity has been identified as an important factor in the pathogenesis of bile duct injury and cholangiopathies. The role of bile salt toxicity in the development of biliary strictures after NHB liver transplantation is unclear.

Methods: In a porcine model of NHB liver transplantation, we studied the effect of different periods of warm ischemia in the donor on bile composition and subsequent bile duct injury after transplantation. After induction of cardiac arrest in the donor, liver procurement was delayed for 0 min (group A), 15 min (group B), or more or equal to 30 min (group C). Livers were subsequently transplanted after 4 hr of cold preservation. In the recipients, bile flow was measured, and bile samples were collected daily to determine the bile salt-to-phospholipid ratio. Severity of bile duct injury was semiquantified by using a histologic grading scale.

Results: Posttransplantation survival was directly related to the duration of warm ischemia in the donor. The bile salt-to-phospholipid ratio in bile produced early after transplantation was significantly higher in group C, compared with group A and B. Histopathologic condition showed the highest degree of bile duct injury in group C.

Conclusion: Prolonged warm ischemia in NHB donors is associated with the formation of toxic bile after transplantation, with a high biliary bile salt-to-phospholipid ratio. These data suggest that bile salt toxicity contributes to the pathogenesis of bile duct injury after NHB liver transplantation.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • ATP Binding Cassette Transporter, Subfamily B / biosynthesis
  • ATP Binding Cassette Transporter, Subfamily B / genetics
  • ATP Binding Cassette Transporter, Subfamily B, Member 11
  • ATP-Binding Cassette Transporters / biosynthesis
  • ATP-Binding Cassette Transporters / genetics
  • Animals
  • Bile Acids and Salts / metabolism
  • Bile Acids and Salts / toxicity*
  • Bile Ducts, Intrahepatic / injuries*
  • Biopsy
  • Cholestasis, Intrahepatic / etiology*
  • Cholestasis, Intrahepatic / metabolism
  • Cholestasis, Intrahepatic / mortality
  • Disease Models, Animal
  • Female
  • Gene Expression
  • Liver Transplantation / adverse effects*
  • Liver Transplantation / mortality
  • Liver Transplantation / pathology
  • RNA, Messenger / genetics
  • Reverse Transcriptase Polymerase Chain Reaction
  • Risk Factors
  • Severity of Illness Index
  • Survival Rate
  • Swine

Substances

  • ATP Binding Cassette Transporter, Subfamily B
  • ATP Binding Cassette Transporter, Subfamily B, Member 11
  • ATP-Binding Cassette Transporters
  • Abcb11 protein, mouse
  • Abcb11 protein, rat
  • Bile Acids and Salts
  • RNA, Messenger
  • multidrug resistance protein 3