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Hypoxia Impairs Endothelial Function in HAPEs

This study has been completed.
Sponsor:
ClinicalTrials.gov Identifier:
NCT00176007
First Posted: September 15, 2005
Last Update Posted: December 9, 2005
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details.
Information provided by:
Heidelberg University
  Purpose
Aim of the study is to investigate the function of the systemic vascular endothelium in individuals susceptible to high-altitude pulmonary oedema during normoxia and normobaric hypoxia.

Condition Intervention Phase
Healthy Procedure: Hypoxia Phase 1

Study Type: Interventional
Study Design: Allocation: Randomized
Intervention Model: Crossover Assignment
Masking: Single
Primary Purpose: Educational/Counseling/Training
Official Title: Hypoxia Impairs Systemic Endothelial Function in Individuals Prone to High-Altitude Pulmonary Edema.

Resource links provided by NLM:


Further study details as provided by Heidelberg University:

Detailed Description:
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.
  Eligibility

Information from the National Library of Medicine

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Ages Eligible for Study:   18 Years to 55 Years   (Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes
Criteria

Inclusion Criteria:

Healthy, male volunteers, age: 18-55

- Able and willing to give written informed consent

Exclusion Criteria:

  • Known condition causing endothelial dysfunction (e.g. diabetes, hyperlipidaemia, arterial hypertension, smoking, hyperhomocysteinaemia)
  • Regular medication and/or treatment with drugs within the last 4 weeks (exclusion has to be decided in each case)
  • Acute or chronic illness
  • Participation in clinical trial/blood donation within 2 month before the study
  • Nicotine, drug and/or alcohol abuse.
  Contacts and Locations
Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT00176007


Sponsors and Collaborators
Heidelberg University
Investigators
Principal Investigator: Walter E Haefeli, MD Heidelberg University
  More Information

ClinicalTrials.gov Identifier: NCT00176007     History of Changes
Other Study ID Numbers: A001
First Submitted: September 10, 2005
First Posted: September 15, 2005
Last Update Posted: December 9, 2005
Last Verified: June 2005

Additional relevant MeSH terms:
Hypoxia
Signs and Symptoms, Respiratory
Signs and Symptoms