Titre
New insights in the pathogenesis of high-altitude pulmonary edema.
Type
synthèse (review)
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Scherrer, Urs
Auteure/Auteur
Rexhaj, Emrush
Auteure/Auteur
Jayet, Pierre-Yves
Auteure/Auteur
Allemann, Yves
Auteure/Auteur
Sartori, Claudio
Auteure/Auteur
Liens vers les personnes
ISSN
1532-8643[electronic], 0033-0620[linking]
Statut éditorial
Publié
Date de publication
2010
Volume
52
Numéro
6
Première page
485
Dernière page/numéro d’article
492
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Résumé
High-altitude pulmonary edema is a life-threatening condition occurring in predisposed but otherwise healthy individuals. It therefore permits the study of underlying mechanisms of pulmonary edema in the absence of confounding factors such as coexisting cardiovascular or pulmonary disease, and/or drug therapy. There is evidence that some degree of asymptomatic alveolar fluid accumulation may represent a normal phenomenon in healthy humans shortly after arrival at high altitude. Two fundamental mechanisms then determine whether this fluid accumulation is cleared or whether it progresses to HAPE: the quantity of liquid escaping from the pulmonary vasculature and the rate of its clearance by the alveolar respiratory epithelium. The former is directly related to the degree of hypoxia-induced pulmonary hypertension, whereas the latter is determined by the alveolar epithelial sodium transport. Here, we will review evidence that, in HAPE-prone subjects, impaired pulmonary endothelial and epithelial NO synthesis and/or bioavailability may represent a central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and, in turn, capillary stress failure and alveolar fluid flooding. We will then demonstrate that exaggerated pulmonary hypertension, although possibly a conditio sine qua non, may not always be sufficient to induce HAPE and how defective alveolar fluid clearance may represent a second important pathogenic mechanism.
Sujets
PID Serval
serval:BIB_993F22EFEDD2
PMID
Date de création
2010-05-26T11:24:21.719Z
Date de création dans IRIS
2025-05-21T03:18:45Z