Endothelin-1 in the rat bile duct ligation model of hepatopulmonary syndrome: Correlation with pulmonary dysfunction

Bao Luo, Gary A. Abrams, Michael B. Fallon

Research output: Contribution to journalArticle

93 Scopus citations

Abstract

Background/Aims: Models of hepatopulmonary syndrome require both hepatic injury and portal hypertension to develop pulmonary microvascular and gas exchange abnormalities. Recently, increased endothelin-1 levels associated with vasodilatation, have been observed in cirrhosis. We investigated endothelin-1 production in common bile duct ligated animals with hepatopulmonary syndrome in comparison to partial portal vein ligated animals that do not develop hepatopulmonary syndrome. Methods: Organ and plasma endothelin-1 were measured in sham, bile duct ligated and portal vein ligated rats, and Northern analysis and immunohistochemistry were performed in liver. Plasma endothelin-1 levels were correlated with pulmonary endothelial nitric oxide synthase levels and alveolar-arterial oxygen gradients. Results: Hepatic and plasma endothelin-1 increased only after bile duct ligation, and were accompanied by increased hepatic endothelin-1 mRNA and increased endothelin-1 protein in biliary epithelium. Plasma endotbelin-1 levels correlated directly with both pulmonary endothelial nitric oxide synthase levels and alveolar-arterial gradients. Conclusions: Enhanced hepatic production and increased plasma levels of endothelin-1 occur after bile duct ligation, but not after portal vein ligation, and correlate with associated molecular and gas exchange alterations in the lung. Endothelin-1 may contribute to the pathogenesis of hepatopulmonary syndrome.

Original languageEnglish (US)
Pages (from-to)571-578
Number of pages8
JournalJournal of Hepatology
Volume29
Issue number4
DOIs
StatePublished - Oct 1998
Externally publishedYes

Keywords

  • Common bile duct ligation
  • Endothelin-1
  • Hepatopulmonary syndrome
  • Portal hypertension

ASJC Scopus subject areas

  • Hepatology

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