Effect of acute hypobaric hypoxia on the endothelial glycocalyx and digital reactive hyperemia in humans.
Effect of acute hypobaric hypoxia on the endothelial glycocalyx and digital reactive hyperemia in humans.
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DOI：
10.3389/fphys.2014.00459
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发表时间：
2014
影响因子：
4
通讯作者：
Olsen NV
中科院分区：
文献类型：
--
作者：
Johansson PI;Bergström A;Aachmann-Andersen NJ;Meyer MA;Ostrowski SR;Nordsborg NB;Olsen NV
Introduction: Hypoxia is associated with increased capillary permeability. This study tested whether acute hypobaric hypoxia involves degradation of the endothelial glycocalyx. Methods: We exposed 12 subjects to acute hypobaric hypoxia (equivalent to 4500 m for 2–4 h) and measured venous blood concentrations of biomarkers reflecting endothelial and glycocalyx degradation (catecholamines, syndecan-1, soluble CD40 ligand, protein C, soluble thrombomodulin, tissue-type plasminogen activators, histone-complexed DNA fragments, and nitrite/nitrate). Endothelial function was assessed by the hyperemic response to brachial artery occlusion by peripheral arterial tonometry. Results: Compared with normoxic baseline levels, hypoxia increased concentrations of syndecan-1 from 22 (95% confidence interval: 17–27) to 25 (19–30) ng/ml (p < 0.02) and protein C from 76 (70–83)% to 81 (74–88)% (p < 0.02). Nitrite/nitrate decreased from 23 (18–27) μM at baseline to 19 (14–24) μM and 18 (14–21) μM in hypoxia and recovery, respectively (p < 0.05). Other biomarkers remained unchanged. The post-occlusion/pre-occlusion ratio (reactive hyperemia index, RHI) decreased from 1.80 (1.52–2.07) in normoxia to 1.62 (1.28–1.96) after 2–4 h of hypobaric hypoxia and thereafter increased to 2.43 (1.99–2.86) during normoxic recovery (p < 0.01). Conclusions: The increase in syndecan-1 and protein C suggests that acute hypobaric hypoxia produces a minor degree of glycocalyx degradation and overall cellular damage. After hypoxia RHI rebounded to higher than baseline levels suggesting improved endothelial functionality.
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影响因子：
10.4
作者：
Johansson, P. I.;Sorensen, A. M.;Ostrowski, S. R.
通讯作者：
Ostrowski, S. R.
DOI：
10.1164/ajrccm.163.2.2001134
发表时间：
2001-02-01
影响因子：
24.7
作者：
Busch, T;Bärtsch, P;Swenson, ER
通讯作者：
Swenson, ER
DOI：
10.1007/978-1-4419-1241-1_3
发表时间：
2010-01-01
期刊：
OXYGEN TRANSPORT TO TISSUE XXXI
影响因子：
--
作者：
Gonzalez, Norberto C.;Wood, John G.
通讯作者：
Wood, John G.
影响因子：
8.3
作者：
Hamburg, Naomi M.;Palmisano, Joseph;Benjamin, Emelia J.
通讯作者：
Benjamin, Emelia J.
影响因子：
5.5
作者：
Bailey, Damian M.;Dehnert, Christoph;Berger, Marc M.
通讯作者：
Berger, Marc M.