Mechanisms and drug therapy of pulmonary hypertension at high altitude.

Détails

ID Serval
serval:BIB_F8E334A3D251
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
Mechanisms and drug therapy of pulmonary hypertension at high altitude.
Périodique
High Altitude Medicine and Biology
Auteur(s)
Scherrer U., Allemann Y., Rexhaj E., Rimoldi S.F., Sartori C.
ISSN
1557-8682 (Electronic)
ISSN-L
1527-0297
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
14
Numéro
2
Pages
126-133
Langue
anglais
Notes
Publication types: Journal ArticlePublication Status: ppublish
Type Pubmed Review
Résumé
Abstract Scherrer, Urs, Yves Allemann, Emrush Rexhaj, Stefano F. Rimoldi, and Claudio Sartori. Mechanisms and drug therapy of pulmonary hypertension at high altitude. High Alt Med Biol 14:126-133, 2013.-Pulmonary vasoconstriction represents a physiological adaptive mechanism to high altitude. If exaggerated, however, it is associated with important morbidity and mortality. Recent mechanistic studies using short-term acute high altitude exposure have provided insight into the importance of defective vascular endothelial and respiratory epithelial nitric oxide (NO) synthesis, increased endothelin-1 bioavailability, and overactivation of the sympathetic nervous system in causing exaggerated hypoxic pulmonary hypertension in humans. Based on these studies, drugs that increase NO bioavailability, attenuate endothelin-1 induced pulmonary vasoconstriction, or prevent exaggerated sympathetic activation have been shown to be useful for the treatment/prevention of exaggerated pulm9onary hypertension during acute short-term high altitude exposure. The mechanisms underpinning chronic pulmonary hypertension in high altitude dwellers are less well understood, but recent evidence suggests that they differ in some aspects from those involved in short-term adaptation to high altitude. These differences have consequences for the choice of the treatment for chronic pulmonary hypertension at high altitude. Finally, recent data indicate that fetal programming of pulmonary vascular dysfunction in offspring of preeclampsia and children generated by assisted reproductive technologies represents a novel and frequent cause of pulmonary hypertension at high altitude. In animal models of fetal programming of hypoxic pulmonary hypertension, epigenetic mechanisms play a role, and targeting of these mechanisms with drugs lowers pulmonary artery pressure. If epigenetic mechanisms also are operational in the fetal programming of pulmonary vascular dysfunction in humans, such drugs may become novel tools for the treatment of hypoxic pulmonary hypertension.
Pubmed
Web of science
Création de la notice
25/06/2013 12:42
Dernière modification de la notice
20/08/2019 16:24
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