title: Simulated temporary hypoxia triggers the release of CD31+/Annexin+ endothelial microparticles: A prospective pilot study in humans.
abstract: BACKGROUND
  Endothelial microparticles (EMP) are small membrane vesicles that originate from activated or apoptotic endothelial cells. Although the exact mechanism of EMP function is still relatively unknown, it has been shown that they modulate inflammatory processes, coagulation and vascular function. In this study we hypothesized that transient hypoxia may act as a trigger for the release of EMP into circulation.
  
  
  METHODS
  Fourteen healthy volunteers were subjected to transient normobaric hypoxia in an air-conditioned chamber simulating an oxygen concentration of a height of up to 5500 meters. Blood samples were evaluated for EMP using flow cytometry.
  
  
  RESULTS
  During the experiment oxygen concentration was adjusted to a value equivalent to a height of 5500 meters to achieve hypoxic conditions. Oxygen saturation decreased to 78% . At the final height a significant increase of CD31+/Annexin+ EMP levels was evident (increase from 0.03% ± 0.01% SEM to 0.12% ± 0.04% SEM, p = 0.0188).
  
  
  CONCLUSIONS
  These experimental results show that temporary hypoxic conditions can trigger the release of CD31+/ Annexin+ EMP also in healthy volunteers. In our previous studies we have shown that apoptotic bodies can confer pro-survival signals to cardiomyocytes during myocardial ischemia. Based on the experimental results of this current study we believe that the release of CD31+/Annexin+ EMP during hypoxia might act as an endogenous survival signal.
authors.affiliation: Clinic of Internal Medicine II, Department of Cardiology, Paracelsus Medical University of Salzburg, Austria.
authors.forename: Michael
authors.initials: M
authors.lastname: Lichtenauer
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Bjoern
authors.initials: B
authors.lastname: Goebel
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Fritzenwanger
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Martin
authors.initials: M
authors.lastname: Förster
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Stefan
authors.initials: S
authors.lastname: Betge
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Alexander
authors.initials: A
authors.lastname: Lauten
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Hans-Reiner
authors.initials: HR
authors.lastname: Figulla
authors.affiliation: Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
authors.forename: Christian
authors.initials: C
authors.lastname: Jung
mesh_terms: D000328:Adult; D017302:Annexins / Q000276:immunology*; D015687:Cell Hypoxia / Q000276:immunology*; D055252:Cell-Derived Microparticles; D042783:Endothelial Cells / Q000276:immunology*; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D008297:Male; D010865:Pilot Projects; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000276:immunology*; D011446:Prospective Studies
chemical_list: D017302:Annexins; D019408:Platelet Endothelial Cell Adhesion Molecule-1
keywords: Hypoxia; endothelial microparticles; human, apoptosis; oxygen saturation