ArticleMetabolic brain disease2021
The pathophysiological mechanism of ischemic stroke after hypobaric hypoxia simulation at high altitude.
Article in Metabolic brain disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- High-altitude hypoxic cues and cerebral ischemic tolerance: an evidence-graded translational framework for stroke research.Frontiers in neuroscience · 2026Review
- The role of orexin A in the pathogenesis of ischaemic stroke at high altitude.Experimental physiology · 2026Article
- Stroke in High-Altitude Areas.Brain and behavior · 2025Review
- Recommendations for traveling to altitude with neurological disorders.Journal of central nervous system disease · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tibet is an area in China with a high incidence of stroke, typically attributed to hypobaric hypoxia. The present study aimed to observe the neuronal injury of ischemic stroke after hypobaric hypoxia and explore the mechanism by which N-methyl-D-aspartate receptor (NMDAR) and its downstream pathways are involved. This study employed a hypobaric chamber to imitate high altitude at 4000 m. After hypoxia, the middle cerebral artery occlusion (MCAO) model was used to mimic ischemic stroke. Behavioral tests and measurements of infarct area were used to observe neuronal injuries. The expression of NMDAR, Ca
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