Viewing Study NCT00176007



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Study NCT ID: NCT00176007
Status: COMPLETED
Last Update Posted: 2005-09-15
First Post: 2005-09-10

Brief Title: Hypoxia Impairs Endothelial Function in HAPEs
Sponsor: Heidelberg University
Organization: Heidelberg University

Study Overview

Official Title: Hypoxia Impairs Systemic Endothelial Function in Individuals Prone to High-Altitude Pulmonary Edema
Status: COMPLETED
Status Verified Date: 2005-06
Last Known Status: None
Delayed Posting: No
If Stopped, Why?: Not Stopped
Has Expanded Access: False
If Expanded Access, NCT#: N/A
Has Expanded Access, NCT# Status: N/A
Acronym: None
Brief Summary: 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
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 FIO2 021 and 4 hours of normobaric hypoxia FIO2 012 corresponding to an altitude of 4500 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 0001 during hypoxia in control subjects and from 25 - 4 to 50 - 9 mm Hg in HAPE-S subjects p 0001 Despite similar responses during normoxia in both groups ACh-induced changes in forearm blood flow markedly decreased during hypoxia in HAPE-S subjects p 001 but not in control subjects The attenuated vascular response to ACh infusion during hypoxia inversely correlated with increased pulmonary artery systolic pressure p 004 and decreased plasma nitrite correlated with attenuated ACh-induced vasodilation in HAPE-S subjects p 002 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

Study Oversight

Has Oversight DMC: None
Is a FDA Regulated Drug?: None
Is a FDA Regulated Device?: None
Is an Unapproved Device?: None
Is a PPSD?: None
Is a US Export?: None
Is an FDA AA801 Violation?: None