title: The role of hemodynamic and vasoactive substances on hepatopulmonary syndrome.
abstract: BACKGROUND
  Hepatopulmonary syndrome (HPS) is a chronic hepatic complication characterized by defect in arterial oxygenation induced by pulmonary vascular dilatation and vasoactive substances in the setting of chronic liver disease (CLD). This study is to investigate the abnormality of hemodynamic and vasoactive substances in hepatopulmonary syndrome.
  
  
  METHODS
  From September 2007 to September 2012, 58 patients with HPS in the General Surgery Department and Transplantation Center of Renji Hospital were enrolled for the case-control study. HPS patients enrolled were referred to as group H, CLD without HPS to as group C and case controls to as group N. Hemodynamic parameters of the systemic and pulmonary circulations as well as vasoactive substances in the radial and pulmonary arteries were measured in all patients. Univariate and multiple regression analysis were performed afterwards.
  
  
  RESULTS
  The mean pulmonary arterial pressure, pulmonary artery wedge pressure, systemic vascular resistance and pulmonary vascular resistance (PVR) in HPS patients were significantly lower than those in CLD patients without HPS (p < 0.05). The nitrite-to-nitrate ratio (NO2-/NO3-), endothelin-1 (ET-1) and tumor necrosis factor-α (TNF-α) in the radial and pulmonary arteries differed significantly among group H, group C and case controls (group N) separately (p < 0.05). The vasoactive intestinal peptide and 6-keto-prostaglandin-F1α in the radial and pulmonary arteries of group H were significantly higher than those in group N (p < 0.05). The NO2(-)/NO3(-) levels correlated negatively with PVR (r = -0.535, p < 0.05) and Endothelin-1 (r = -0.624, p < 0.05). CO (p < 0.05), CI (p < 0.05), SI (p < 0.05) and TNF-α (p < 0.05) level are considered significantly when performed with multiple regression analysis.
  
  
  CONCLUSIONS
  The CO increases and PVR decreases in HPS patients. The abnormally elevated NO2-/NO3- level in the pulmonary circulation leads to pulmonary vasodilation. ET-1 may induce nitric oxide synthesis and correlated negatively with PVR in HPS. CO, CI, SI and TNF-α level are independent risk factors for HPS patients' survival.
authors.affiliation: Department of General Surgery, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Pudong, Shanghai, China. huarong1017@126.com.
authors.forename: G
authors.initials: G
authors.lastname: Feng
authors.forename: H
authors.initials: H
authors.lastname: Rong
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood / Q000378:metabolism; D016022:Case-Control Studies; D019332:Endothelin-1 / Q000097:blood / Q000378:metabolism; D005260:Female; D006439:Hemodynamics / Q000502:physiology*; D020065:Hepatopulmonary Syndrome / Q000097:blood* / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism; D011651:Pulmonary Artery / Q000378:metabolism / Q000503:physiopathology; D011652:Pulmonary Circulation / Q000502:physiology*; D017534:Radial Artery / Q000378:metabolism / Q000503:physiopathology; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology; D014660:Vasoactive Intestinal Peptide / Q000097:blood / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology*
chemical_list: D019332:Endothelin-1; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D014660:Vasoactive Intestinal Peptide; D015121:6-Ketoprostaglandin F1 alpha