Remote ischemic preconditioning delays the onset of acute mountain sickness in normobaric hypoxia

Acute mountain sickness (AMS) is a neurological disorder occurring when ascending too fast, too high. Remote ischemic preconditioning (RIPC) is a noninvasive intervention protecting remote organs from subsequent hypoxic damage. We hypothesized that RIPC protects against AMS and that this effect is r...

Full description

Saved in:
Bibliographic Details
Published inPhysiological reports Vol. 3; no. 3; pp. e12325 - n/a
Main Authors Berger, Marc M., Köhne, Hannah, Hotz, Lorenz, Hammer, Moritz, Schommer, Kai, Bärtsch, Peter, Mairbäurl, Heimo
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.03.2015
BlackWell Publishing Ltd
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Acute mountain sickness (AMS) is a neurological disorder occurring when ascending too fast, too high. Remote ischemic preconditioning (RIPC) is a noninvasive intervention protecting remote organs from subsequent hypoxic damage. We hypothesized that RIPC protects against AMS and that this effect is related to reduced oxidative stress. Fourteen subjects were exposed to 18 hours of normoxia (21% oxygen) and 18 h of normobaric hypoxia (12% oxygen, equivalent to 4500 m) on different days in a blinded, randomized order. RIPC consisted of four cycles of lower limb ischemia (5 min) and 5 min of reperfusion, and was performed immediately before the study room was entered. A control group was exposed to hypoxia (12% oxygen, n = 14) without RIPC. AMS was evaluated by the Lake Louise score (LLS) and the AMS‐C score of the Environmental Symptom Questionnaire. Plasma concentrations of ascorbate radicals, oxidized sulfhydryl (SH) groups, and electron paramagnetic resonance (EPR) signal intensity were measured as biomarkers of oxidative stress. RIPC reduced AMS scores (LLS: 1.9 ± 0.4 vs. 3.2 ± 0.5; AMS‐C score: 0.4 ± 0.1 vs. 0.8 ± 0.2), ascorbate radicals (27 ± 7 vs. 65 ± 18 nmol/L), oxidized SH groups (3.9 ± 1.4 vs. 14.3 ± 4.6 μmol/L), and EPR signal intensity (0.6 ± 0.2 vs. 1.5 ± 0.4 × 106) after 5 h in hypoxia (all P < 0.05). After 18 hours in hypoxia there was no difference in AMS and oxidative stress between RIPC and control. AMS and plasma markers of oxidative stress did not correlate. This study demonstrates that RIPC transiently reduces symptoms of AMS and that this effect is not associated with reduced plasma levels of reactive oxygen species. Acute mountain sickness (AMS) is a neurological disorder occurring when ascending too fast, too high. Remote ischemic preconditioning (RIPC) is a noninvasive intervention protecting remote organs from subsequent hypoxic damage. The present prospective, randomized, and controlled study shows for the first time that RIPC, induced by transient lower limb ischemia, reduced symptoms of AMS after 5 h but not after 18 h of exposure to normobaric hypoxia at an FiO2 corresponding to an altitude of 4500 m.
Bibliography:No funding information provided.
Funding Information
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
The study was performed at the University Hospital, Heidelberg.
Member of the German Center for Lung Research (DZL).
Funding Information No funding information provided.
ISSN:2051-817X
2051-817X
DOI:10.14814/phy2.12325