title: Soluble selectins in the pulmonary and systemic circulation in acute cardiogenic and non-cardiogenic pulmonary failure.
abstract: OBJECTIVE
  Pulmonary endothelial activation caused by high pulmonary capillary pressures may be involved in the pathogenesis of cardiogenic pulmonary edema (CPE). We studied soluble selectins and soluble ICAM-1 as markers of cell activation in the systemic and pulmonary circulation of patients with respiratory failure (RF) due to CPE (RFCPE) as compared to patients with RF due to pulmonary infection (RFPI).
  
  
  METHODS
  Cardiovascular Intensive Care Unit at a university hospital.
  
  
  METHODS
  Twenty patients with RFCPE, 20 patients with RFPI and 17 critically ill patients without RF.
  
  
  METHODS
  Blood samples were obtained from the arterial and the pulmonary capillary circulation and sE-, sL-, and sP-selectin as well as sICAM-1 were determined. To distinguish between systemic and pulmonary endothelial activation, transpulmonary gradients (concentrationarterial blood - concentrationpulmonary capillary blood) were calculated.
  
  
  RESULTS
  Systemic concentration of sL-selectin was lower in patients with RFCPE and RFPI than in patients without RF (RFCPE: 719.0 +/- 243.9 ng/ml, RFPI: 528.5 +/- 220.8 ng/ml, no RF: 882.4 +/- 222.6 ng/ml; P < 0.001). Systemic concentrations of ICAM-1, sE- and sP-selectin were not significantly different between the three groups. Transpulmonary gradients in sE- and sL-selectin were predominantly negative in patients with RFCPE (-3.2 +/- 7.8 ng/ml and -55.4 +/- 116.1 ng/ml, respectively) and RFPI (-2.3 +/- 5.8 ng/ml and -17.6 +/- 40.3 ng/ml, respectively) but were predominantly positive in patients without RF (11.6 +/- 7.2 ng/ml and 66.6 +/- 69.6 ng/ml, respectively), which suggests trapping of sE- and sL-selectin in the pulmonary circulation in the majority of patients with RFPI as well as in the majority of patients with RFCPE.
  
  
  CONCLUSIONS
  Pulmonary endothelial activation occurs during both RFCPE and RFPI. This adds evidence that, besides hydrostatic mechanisms, cell activation occurs during CPE.
authors.affiliation: Intensive Care Unit, Department of Cardiology, University of Vienna, AKH, Währinger Gürtel 18-20, 1090 Vienna, Austria. Alexander.Geppert@univie.ac.at
authors.forename: A
authors.initials: A
authors.lastname: Geppert
authors.forename: G
authors.initials: G
authors.lastname: Zorn
authors.forename: G
authors.initials: G
authors.lastname: Heinz
authors.forename: K
authors.initials: K
authors.lastname: Huber
authors.forename: P
authors.initials: P
authors.lastname: Siostrzonek
mesh_terms: D000208:Acute Disease; D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000276:immunology; D005260:Female; D006333:Heart Failure / Q000150:complications*; D006801:Humans; D007239:Infections / Q000150:complications*; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood*; D008171:Lung Diseases / Q000150:complications*; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000150:complications*; D011669:Pulmonary Wedge Pressure; D012131:Respiratory Insufficiency / Q000097:blood / Q000209:etiology* / Q000276:immunology* / Q000401:mortality / Q000503:physiopathology; D019087:Selectins / Q000097:blood*; D016019:Survival Analysis
chemical_list: D015415:Biomarkers; D019087:Selectins; D018799:Intercellular Adhesion Molecule-1