| Hypoxia impairs systemic endothelial function in individuals prone to high-altitude pulmonary edema. | |
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MedLine Citation:
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PMID: 15947284 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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RATIONALE: High-altitude pulmonary edema (HAPE) is characterized by excessive pulmonary vasoconstriction and is associated with decreased concentrations of nitric oxide (NO) in the lung. Objectives: We hypothesized that individuals susceptible to HAPE (HAPE-S) would also have dysfunction of the vascular NO vasodilator pathway during hypoxia in the systemic vasculature. METHODS: During normoxia (FI(O(2)) = 0.21) and 4 hours of normobaric hypoxia (FI(O(2)) = 0.12, corresponding to an altitude of 4,500 m above sea level) endothelium-dependent and endothelium-independent vasodilator responses to intraarterial infusion of acetylcholine (ACh) and sodium nitroprusside, respectively, were measured by forearm venous occlusion plethysmography in nine HAPE-S subjects and in nine HAPE-resistant control subjects. MAIN RESULTS: Pulmonary artery systolic pressure increased from 22 +/- 3 to 33 +/- 6 mm Hg (p < 0.001) during hypoxia in control subjects, and from 25 +/- 4 to 50 +/- 9 mm Hg in HAPE-S subjects (p < 0.001). Despite similar responses during normoxia in both groups, ACh-induced changes in forearm blood flow markedly decreased during hypoxia in HAPE-S subjects (p = 0.01) but not in control subjects. The attenuated vascular response to ACh infusion during hypoxia inversely correlated with increased pulmonary artery systolic pressure (p = 0.04) and decreased plasma nitrite correlated with attenuated ACh-induced vasodilation in HAPE-S subjects (p = 0.02). CONCLUSIONS: Hypoxia markedly impairs vascular endothelial function in the systemic circulation in HAPE-S subjects due to a decreased bioavailability of NO. Impairment of the NO pathway could contribute to the enhanced hypoxic pulmonary vasoconstriction that is central to the pathogenesis of HAPE. |
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Authors:
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Marc M Berger; Christiane Hesse; Christoph Dehnert; Heike Siedler; Petra Kleinbongard; Hubert J Bardenheuer; Malte Kelm; Peter Bärtsch; Walter E Haefeli |
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Publication Detail:
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Type: Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't Date: 2005-06-09 |
Journal Detail:
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Title: American journal of respiratory and critical care medicine Volume: 172 ISSN: 1073-449X ISO Abbreviation: Am. J. Respir. Crit. Care Med. Publication Date: 2005 Sep |
Date Detail:
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Created Date: 2005-09-08 Completed Date: 2005-11-15 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9421642 Medline TA: Am J Respir Crit Care Med Country: United States |
Other Details:
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Languages: eng Pagination: 763-7 Citation Subset: AIM; IM |
Affiliation:
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Department of Internal Medicine VI (Clinical Pharmacology and Pharmacoepidemiology), University of Heidelberg, Germany. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Adult Altitude Sickness / etiology* Anoxia / blood, physiopathology* Blood Pressure Disease Susceptibility Endothelin-1 / blood Endothelium, Vascular / physiopathology* Female Forearm / blood supply Hemodynamics Humans Male Middle Aged Nitrates / blood Nitrites / blood Nitroprusside / pharmacology Pulmonary Artery / physiopathology Pulmonary Edema / etiology* Pulmonary Gas Exchange Regional Blood Flow Single-Blind Method Vasodilation Vasodilator Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Endothelin-1; 0/Nitrates; 0/Nitrites; 0/Vasodilator Agents; 15078-28-1/Nitroprusside; 51-84-3/Acetylcholine |
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