ArticleExperimental and therapeutic medicine2015
Effect of hyperbaric oxygen preconditioning on peri-hemorrhagic focal edema and aquaporin-4 expression.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Aquaporins in Acute Brain Injury: Insights from Clinical and Experimental Studies.Biomedicines · 2025Review
- The Glymphatic System: A Novel Therapeutic Target for Stroke Treatment.Frontiers in aging neuroscience · 2021Review
- Review
- Hyperbaric oxygen preconditioning attenuates brain injury after intracerebral hemorrhage by regulating microglia polarization in rats.CNS neuroscience & therapeutics · 2019Article
- A Dual Role for Hyperbaric Oxygen in Stroke Neuroprotection: Preconditioning of the Brain and Stem Cells.Conditioning medicine · 2018Article
- The efficacy of hyperbaric oxygen in hemorrhagic stroke: experimental and clinical implications.Archives of medical science : AMS · 2017Article
- Current AQP research: therapeutic approaches to ischemic and hemorrhagic stroke.Neural regeneration research · 2016Article
- Aquaporin-4 and Cerebrovascular Diseases.International journal of molecular sciences · 2016Review
- Progress in AQP Research and New Developments in Therapeutic Approaches to Ischemic and Hemorrhagic Stroke.International journal of molecular sciences · 2016Review
- Hyperbaric oxygen preconditioning: a reliable option for neuroprotection.Medical gas research · 2016Review
- Medical gases for stroke therapy: summary of progress 2015-2016.Medical gas researchReview
- Combined application of hypothermia and medical gases in cerebrovascular diseases.Medical gas researchReview
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate the effect of hyperbaric oxygen preconditioning (HBO-PC) on peri-hemorrhagic focal edema and aquaporin-4 (AQP-4) expression in an experimental intracerebral hemorrhage (ICH) rat model. Sixty-six Sprague Dawley® rats were divided into three groups: The sham-surgery group (SHG; n=6); the control group (A-ICH; n=30), in which the rats were injected with autologous blood; and the experimental HBO-PC group (P-HBO; n=30). The rats underwent brain edema and AQP-4 detection at 5 postoperative time-points (24, 48 and 72 h and 5 and 7 days). The water content in the brain tissues of the A-ICH animals was higher than that in the brain tissues of the SHG rats at each time-point (P<0.05), and the edema in the P-HBO was significantly more severe 24 and 48 h postoperatively than that at 7 days postoperatively (P<0.05). The difference between the P-HBO and A-ICH was significant at 48 and 72 h postoperatively (P<0.05). AQP-4 was expressed in the post-hemorrhagic rat brains of all groups; the SHG animals exhibited low expression, while the A-ICH animals exhibited an increased expression 24 h postoperatively. In the A-ICH, expression peaked at 48 h postoperatively and began to decrease gradually after 72 h. At the 7-day time-point, the expression level in the A-ICH was closer to but still higher than that of the SHG animals (P<0.05). The differences between the P-HBO and A-ICH animals at the postoperative 24-h, 48-h and 7-day time-points were statistically significant (P<0.05). In conclusion, HBO-PC may downregulate AQP-4 expression to reduce the intracerebral edema, thus strengthening tolerance to ICH and protecting the nerves.
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