Lichtenauer Michael, Goebel Bjoern, Fritzenwanger Michael, Förster Martin, Betge Stefan, Lauten Alexander, Figulla Hans-Reiner, Jung Christian
Clinic of Internal Medicine II, Department of Cardiology, Paracelsus Medical University of Salzburg, Austria.
Universitätsherzzentrum Thüringen, Clinic of Internal Medicine I, Department of Cardiology, Friedrich Schiller University Jena, Germany.
Clin Hemorheol Microcirc. 2015;61(1):83-90. doi: 10.3233/CH-141908.
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.
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.
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).
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.
内皮微粒（EMP）是源自活化或凋亡内皮细胞的小膜泡。尽管EMP功能的确切机制仍相对不明，但已表明它们可调节炎症过程、凝血和血管功能。在本研究中，我们假设短暂缺氧可能是EMP释放到循环中的触发因素。
14名健康志愿者在模拟高达5500米高度氧气浓度的空调舱中接受短暂常压缺氧。使用流式细胞术评估血样中的EMP。
在实验期间，将氧气浓度调整到相当于5500米高度的值以实现缺氧条件。血氧饱和度降至78%。在最终高度时，CD31+/膜联蛋白+ EMP水平显著增加（从0.03%±0.01% SEM增加到0.12%±0.04% SEM，p = 0.0188）。
这些实验结果表明，临时缺氧条件也可在健康志愿者中触发CD31+/膜联蛋白+ EMP的释放。在我们之前的研究中，我们已表明凋亡小体可在心肌缺血期间赋予心肌细胞促生存信号。基于本研究的实验结果，我们认为缺氧期间CD31+/膜联蛋白+ EMP的释放可能作为一种内源性生存信号。
