Hypoxia impairs systemic endothelial function in individuals prone to high-altitude pulmonary edema
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 vasc...
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| Main Authors: | , , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
June 9, 2005
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| In: |
American journal of respiratory and critical care medicine
Year: 2005, Volume: 172, Issue: 6, Pages: 763-767 |
| ISSN: | 1535-4970 |
| DOI: | 10.1164/rccm.200504-654OC |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1164/rccm.200504-654OC Verlag, lizenzpflichtig, Volltext: https://www.atsjournals.org/doi/full/10.1164/rccm.200504-654OC 
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| Author Notes: | Marc M. Berger, Christiane Hesse, Christoph Dehnert, Heike Siedler, Petra Kleinbongard, Hubert J. Bardenheuer, Malte Kelm, Peter Bärtsch, and Walter E. Haefeli |
MARC
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| 245 | 1 | 0 | |a Hypoxia impairs systemic endothelial function in individuals prone to high-altitude pulmonary edema |c Marc M. Berger, Christiane Hesse, Christoph Dehnert, Heike Siedler, Petra Kleinbongard, Hubert J. Bardenheuer, Malte Kelm, Peter Bärtsch, and Walter E. Haefeli |
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| 520 | |a 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 (FIO2 = 0.21) and 4 hours of normobaric hypoxia (FIO2 = 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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