title: Plasma markers of endothelial dysfunction in pulmonary hypertension.
abstract: OBJECTIVE
  To evaluate and to correlate endothelial cell dysfunction, using recently available plasma markers, with the magnitude of pulmonary artery pressure in patients with severe pulmonary hypertension (PH).
  
  
  METHODS
  Selected plasma markers of endothelial cell dysfunction were studied: nitric oxide (NO), thrombomodulin, tissue factor pathway inhibitor, and soluble endothelium, leukocyte, and platelet selectins (sE-, sL-, sP-selectins, respectively).
  
  
  METHODS
  Padova University Hospital and Department of Pathology and Pharmacology, Loyola University of Chicago, Chicago, IL.
  
  
  METHODS
  Fifteen patients had severe PH (four men and 11 women; mean age, 49.7 +/- 2.9 years: seven patients had primary pulmonary hypertension [PPH] and eight patients had secondary pulmonary hypertension [SPH]), and 20 patients were healthy control subjects.
  
  
  RESULTS
  In patients with PH, sP- and sE-selectins were elevated, whereas sL-selectin was lower in comparison with the selectin levels in control subjects. However, the differences between patients with PH and control subjects were significant only for sL-selectin (p < 0.0001) and sE-selectin (p < 0.03). The NO level was significantly lower in patients with PH compared with the NO level in control subjects (p < 0.01). No difference in tissue factor pathway inhibitor level was noted between control subjects and patients with PH. Only a weak correlation was found between thrombomodulin plasma levels and magnitude of systolic pulmonary artery pressure (r = -0.528, p < 0.05).
  
  
  CONCLUSIONS
  Our data are in keeping with the evidence for significant endothelial cell dysfunction in patients with PH and the need for chronic anticoagulation believed to increase survival in these patients. In addition, these data seem to suggest a need for newer agents that are able to increase the antithrombotic endothelial function.
authors.affiliation: Department of Medical and Surgical Sciences, University of Padova, Medical School, Padova, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Cella
authors.forename: F
authors.initials: F
authors.lastname: Bellotto
authors.forename: F
authors.initials: F
authors.lastname: Tona
authors.forename: A
authors.initials: A
authors.lastname: Sbarai
authors.forename: G
authors.initials: G
authors.lastname: Mazzaro
authors.forename: G
authors.initials: G
authors.lastname: Motta
authors.forename: J
authors.initials: J
authors.lastname: Fareed
mesh_terms: D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006976:Hypertension, Pulmonary / Q000097:blood*; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000097:blood*; D011379:Prognosis; D011651:Pulmonary Artery / Q000503:physiopathology; D012016:Reference Values; D019087:Selectins / Q000097:blood*; D018180:Thrombomodulin / Q000097:blood*
chemical_list: D008074:Lipoproteins; D019087:Selectins; D018180:Thrombomodulin; C051928:lipoprotein-associated coagulation inhibitor; D009569:Nitric Oxide