Edema pulmonar de altura. Modelo de estudio de la fisiopatologia del edema pulmonar y de la hipertension pulmonar hipoxica en humanos [High altitude pulmonary edema. An experiment of nature to study the underlying mechanisms of hypoxic pulmonary hypertension and pulmonary edema in humans]

Détails

ID Serval
serval:BIB_50E4E83FD760
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Edema pulmonar de altura. Modelo de estudio de la fisiopatologia del edema pulmonar y de la hipertension pulmonar hipoxica en humanos [High altitude pulmonary edema. An experiment of nature to study the underlying mechanisms of hypoxic pulmonary hypertension and pulmonary edema in humans]
Périodique
Medicina
Auteur(s)
Schwab M., Jayet P.Y., Allemann Y., Sartori C., Scherrer U.
ISSN
0025-7680
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
67
Numéro
1
Pages
71-81
Notes
Publication types: English Abstract ; Journal Article ; Review
Résumé
High altitude constitutes an exciting natural laboratory for medical research. Over the past decade, it has become clear that the results of high-altitude research may have important implications not only for the understanding of diseases in the millions of people living permanently at high altitude, but also for the treatment of hypoxemia-related disease states in patients living at low altitude. High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed, but otherwise healthy subjects, and, therefore, allows to study underlying mechanisms of pulmonary edema in humans, in the absence of confounding factors. Over the past decade, evidence has accumulated that HAPE results from the conjunction of two major defects, augmented alveolar fluid flooding resulting from exaggerated hypoxic pulmonary hypertension, and impaired alveolar fluid clearance related to defective respiratory transepithelial sodium transport. Here, after a brief presentation of the clinical features of HAPE, we review this novel concept. We provide experimental evidence for the novel concept that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent the central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and alveolar fluid flooding. We demonstrate that exaggerated pulmonary hypertension, while possibly a condition sine qua non, may not be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we outline how this insight gained from studies in HAPE may be translated into the management of hypoxemia related disease states in general.
Mots-clé
Altitude Sickness, Biological Availability, Biological Transport, Blood Pressure, Epithelial Sodium Channel, Humans, Hypertension, Pulmonary, Nitric Oxide, Pulmonary Alveoli, Pulmonary Circulation, Pulmonary Edema, Sodium, Sympathetic Nervous System
Pubmed
Web of science
Création de la notice
22/02/2008 16:02
Dernière modification de la notice
03/03/2018 17:09
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