Simulated temporary hypoxia triggers the release of CD31+/Annexin+ endothelial microparticles: A prospective pilot study in humans

Article type: Research Article

Authors: Lichtenauer, Michael^a | Goebel, Bjoern^b | Fritzenwanger, Michael^b | Förster, Martin^b | Betge, Stefan^b | Lauten, Alexander^b | Figulla, Hans-Reiner^b | Jung, Christian^{b; *}

Affiliations: [a] Clinic of Internal Medicine II, Department of Cardiology, Paracelsus Medical University of Salzburg, Austria | [b] Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany

Correspondence: [*] Corresponding author: Christian Jung, MD, Universitätsherzzentrum Thüringen Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany Erlanger Allee 101, 07747 Jena, Germany. Tel.: +49 3641 9 324559; Fax: +49 3641 9 324102; E-mail: [email protected]

Abstract: INTRODUCTION: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. MATERIALS AND 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.

Keywords: Hypoxia, endothelial microparticles, human, apoptosis, oxygen saturation

DOI: 10.3233/CH-141908

Journal: Clinical Hemorheology and Microcirculation, vol. 61, no. 1, pp. 83-90, 2015