ArticleStroke2015
Normobaric hyperoxia slows blood-brain barrier damage and expands the therapeutic time window for tissue-type plasminogen activator treatment in cerebral ischemia.
Article in Stroke, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04144868 (Normobaric Hyperoxia for Intracerebral Hemorrhage A Randomized Clinical Trial), which is not on this map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Normobaric Hyperoxia for Intracerebral Hemorrhage A Randomized Clinical Trial
Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Pooled it
- Trial
- Enhancing Blood-Brain Barrier Integrity in Patients With Acute Ischemic Stroke Via Normobaric Hyperoxia.Journal of the American Heart Association · 2024Trial
- Normobaric oxygen may correct chronic cerebral ischemia-mediated EEG anomalies.CNS neuroscience & therapeutics · 2021Trial
- Precision Oxygen Modulation in the Reperfusion Era: Conditioning and Therapeutic Strategies in Ischemic Stroke.Journal of stroke · 2026Review
- Neuroinflammation and blood-brain barrier dysfunction in cerebral small vessel disease: mechanisms, biomarkers, and therapeutic implications.European journal of medical research · 2026Review
- Multimodal Neuroprotection in Ischemic Stroke: Emerging Non-Pharmacological Interventions from Bench to Bedside.Brain sciences · 2025Review
- Normobaric Hyperoxia Therapy in Treating Stroke.Clinical interventions in aging · 2025Review
- The neuroprotective effects of normobaric oxygen therapy after stroke.CNS neuroscience & therapeutics · 2024Review
- Exposure to hyperbaric OFluids and barriers of the CNS · 2024Article
- Nuclear Factor Erythroid 2-Related Factor 2 is Essential for Low-Normobaric Oxygen Treatment-Mediated Blood-Brain Barrier Protection Following Ischemic Stroke.Molecular neurobiology · 2024Article
- Opportunities for Neuroprotective Drugs in the Era of Vascular Recanalization.Translational stroke research · 2024Article
- Normobaric hyperoxia alleviates complement C3-mediated synaptic pruning and brain injury after intracerebral hemorrhage.CNS neuroscience & therapeutics · 2024Article
- Review
- Pyruvate Dehydrogenase Complex in Neonatal Hypoxic-Ischemic Brain Injury.ACS pharmacology & translational science · 2024Review
- Normobaric Hyperoxia (NBHO): An Adjunctive Therapy to Cerebrovascular Recanalization in Ischemic Stroke.Aging and disease · 2023Article
- Cerebral Oxygen Delivery and Consumption in Brain-Injured Patients.Journal of personalized medicine · 2022Review
- Normobaric hyperoxia plays a neuroprotective role after cerebral ischemia by maintaining the redox homeostasis and the level of connexin43 in astrocytes.CNS neuroscience & therapeutics · 2022Article
- Application time and persistence of transcranial direct current stimulation (tDCS) against neuronal death resulting from transient cerebral ischemia.Laboratory animal research · 2022Article
- Hemorrhagic Transformation After Tissue Plasminogen Activator Treatment in Acute Ischemic Stroke.Cellular and molecular neurobiology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeProlonged ischemia causes blood-brain barrier (BBB) damage and increases the incidence of neurovasculature complications secondary to reperfusion. Therefore, targeting ischemic BBB damage pathogenesis is critical to reducing neurovasculature complications and expanding the therapeutic time window of tissue-type plasminogen activator (tPA) thrombolysis. This study investigates whether increasing cerebral tissue PO2 through normobaric hyperoxia (NBO) treatment will slow the progression of BBB damage and, thus, improve the outcome of delayed tPA treatment after cerebral ischemia.
methodsRats were exposed to NBO (100% O2) or normoxia (21% O2) during 3-, 5-, or, 7-hour middle cerebral artery occlusion. Fifteen minutes before reperfusion, tPA was continuously infused to rats for 30 minutes. Neurological score, mortality rate, and BBB permeability were determined. Matrix metalloproteinase-9 was measured by gelatin zymography and tight junction proteins (occludin and cluadin-5) by Western blot in the isolated cerebral microvessels.
resultsNBO slowed the progression of ischemic BBB damage pathogenesis, evidenced by reduced Evan blue leakage, smaller edema, and hemorrhagic volume in NBO-treated rats. NBO treatment reduced matrix metalloproteinase-9 induction and the loss of tight junction proteins in ischemic cerebral microvessels. NBO-afforded BBB protection was maintained during tPA reperfusion, resulting in improved neurological functions, significant reductions in brain edema, hemorrhagic volume, and mortality rate, even when tPA was given after prolonged ischemia (7 hours).
conclusionsEarly NBO treatment slows ischemic BBB damage pathogenesis and significantly improves the outcome of delayed tPA treatment, providing new evidence supporting NBO as an effective adjunctive therapy to extend the time window of tPA thrombolysis for ischemic stroke.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.