title: Endothelial selectins in acute mountain sickness and high-altitude pulmonary edema.
abstract: OBJECTIVE
  Mechanical or inflammatory injury to pulmonary endothelial cells may cause impaired pulmonary gas exchange in acute mountain sickness (AMS) and noncardiogenic pulmonary edema in high-altitude pulmonary edema (HAPE). This study was designed to determine whether markers of endothelial cell activation or injury, plasma E- and P-selectin, were increased after ascent to high altitude, in AMS or in HAPE.
  
  
  METHODS
  We collected clinical data and plasma specimens in control subjects at sea level and after ascent to 4,200 m, and in climbers with AMS or HAPE at 4,200 m. Data analysis was performed using standard nonparametric statistical methods, and results reported as mean+/-SD.
  
  
  METHODS
  National Park Service medical camp at 4,200 m on Mt. McKinley (Denali), Alaska.
  
  
  METHODS
  Blood samples and clinical data were collected from 17 healthy climbers at sea level and again after ascent to 4,200 m, and from a different group of 13 climbers with AMS and 8 climbers with HAPE at 4,200 m. Climbers with AMS were divided into normoxic (n=7) and hypoxemic (n=6) groups.
  
  
  RESULTS
  Using an enzyme immunoassay technique, plasma E-selectin concentrations were found to be increased in the 17 control subjects after ascent to 4,200 m (17.2+/-8.2 ng/mL) as compared to sea level (12.9+/-8.2 ng/mL) (p=0.001). Plasma E-selectin concentrations were also increased in subjects with hypoxemic AMS (30.6+/-13.4 ng/mL) and HAPE (23.3+/-9.1 ng/mL) compared to control subjects at sea level (p=0.009). Increased plasma E-selectin concentration significantly correlated with hypoxemia (p=0.006). Plasma P-selectin concentrations were unchanged after ascent to 4,200 m and in subjects with AMS and HAPE.
  
  
  CONCLUSIONS
  Because E-selectin is produced only by endothelial cells, increased plasma E-selectin after ascent to high altitude and in hypoxemic climbers with AMS and HAPE provides evidence that endothelial cell activation or injury is a component of hypoxic altitude illness.
authors.affiliation: Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, USA. ldcgriss@ihc.com
authors.forename: C K
authors.initials: CK
authors.lastname: Grissom
authors.forename: G A
authors.initials: GA
authors.lastname: Zimmerman
authors.forename: R E
authors.initials: RE
authors.lastname: Whatley
mesh_terms: D000208:Acute Disease; D000328:Adult; D000413:Alaska; D000532:Altitude Sickness / Q000097:blood*; D019040:E-Selectin / Q000097:blood*; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods / Q000706:statistics & numerical data; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009051:Mountaineering; D019007:P-Selectin / Q000097:blood*; D011654:Pulmonary Edema / Q000097:blood*; D012995:Solubility; D013048:Specimen Handling / Q000379:methods; D018709:Statistics, Nonparametric
chemical_list: D019040:E-Selectin; D019007:P-Selectin