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Endothelial Selectins in Acute Mountain Sickness and High-Altitude Pulmonary Edema

Colin K. Grissom; Guy A. Zimmerman; Ralph E. Whatley
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Affiliations: From the Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City; the Denali Medical Research Project, Mt. McKinley, Alaska,  From the Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City,  From the Pulmonary and Critical Care Medicine Section, Department of Medicine, East Carolina School of Medicine, Greenville, NC.

Affiliations: From the Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City; the Denali Medical Research Project, Mt. McKinley, Alaska,  From the Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City,  From the Pulmonary and Critical Care Medicine Section, Department of Medicine, East Carolina School of Medicine, Greenville, NC.

Affiliations: From the Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City; the Denali Medical Research Project, Mt. McKinley, Alaska,  From the Pulmonary Division and the Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City,  From the Pulmonary and Critical Care Medicine Section, Department of Medicine, East Carolina School of Medicine, Greenville, NC.


1997 by the American College of Chest Physicians


Chest. 1997;112(6):1572-1578. doi:10.1378/chest.112.6.1572
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Abstract

Study objectives: 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.

Design: 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.

Setting: National Park Service medical camp at 4,200 m on Mt. McKinley (Denali), Alaska.

Patients: 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.

Measurements and 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.

Conclusion: 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.


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