ArticleTranslational stroke research2012
Inhibition of carbonic anhydrase reduces brain injury after intracerebral hemorrhage.
Article in Translational stroke research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 68 citations in OpenAlex.
- Global Prevalence of Sleep-Disordered Breathing in Intracerebral Hemorrhage Survivors: A Meta-Analysis and Systematic Review.Neurology international · 2026Review
- Applications of Carbonic Anhydrase Inhibitors in Arthritis, Neuropathic Pain, Acute Mountain Sickness, and Cerebral Ischemia.Sub-cellular biochemistry · 2026Review
- RADAR - Radiomics on aSDH: predicting outcome with surface area.Acta neurochirurgica · 2025Article
- Exploring the Constituents and Mechanisms ofCombinatorial chemistry & high throughput screening · 2025Article
- Metabolic Pathways in Hydrocephalus: Profiling with Proteomics and Advanced Imaging.Metabolites · 2024Review
- Intracerebral hemorrhage-induced brain injury in mice: The role of peroxiredoxin 2-Toll-like receptor 4 inflammatory axis.CNS neuroscience & therapeutics · 2024Article
- Influence of Blood Components on Neuroinflammation, Blood-Brain Barrier Breakdown, and Functional Damage After Acute Subdural Hematoma in Rats.Neurotrauma reports · 2024Article
- Hydrocephalus is an independent factor affecting morbidity and mortality of ICH patients: Systematic review and meta-analysis.World neurosurgery: X · 2023Review
- Brain edema formation and therapy after intracerebral hemorrhage.Neurobiology of disease · 2023Review
- The Fate of Erythrocytes after Cerebral Hemorrhage.Translational stroke research · 2022Review
- Acetazolamide modulates intracranial pressure directly by its action on the cerebrospinal fluid secretion apparatus.Fluids and barriers of the CNS · 2022Article
- Mechanisms of neuroinflammation in hydrocephalus after intraventricular hemorrhage: a review.Fluids and barriers of the CNS · 2022Review
- The Role of Peroxiredoxins in the Regulation of Sepsis.Antioxidants (Basel, Switzerland) · 2022Review
- Sphingosine-1-phosphate receptor 3 is implicated in BBB injury via the CCL2-CCR2 axis following acute intracerebral hemorrhage.CNS neuroscience & therapeutics · 2021Article
- Role of Carbonic Anhydrase in Cerebral Ischemia and Carbonic Anhydrase Inhibitors as Putative Protective Agents.International journal of molecular sciences · 2021Review
- Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang.Frontiers in cellular neuroscience · 2021Article
- Proteomics-Based Approach to Identify Novel Blood Biomarker Candidates for Differentiating Intracerebral Hemorrhage From Ischemic Stroke-A Pilot Study.Frontiers in neurology · 2021Article
- Carbonic Anhydrases as Potential Targets Against Neurovascular Unit Dysfunction in Alzheimer's Disease and Stroke.Frontiers in aging neuroscience · 2021Review
- Intracerebral Hemorrhage-Induced Brain Injury in Rats: the Role of Extracellular Peroxiredoxin 2.Translational stroke research · 2020Article
- The Blood Component Iron Causes Neuronal Apoptosis Following Intracerebral Hemorrhage via the PERK Pathway.Frontiers in neurology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Carbonic anhydrase-1 (CA-1) is a metalloenzyme present at high concentrations in erythrocytes. Our previous studies showed that erythrocyte lysis contributes to brain edema formation after intracerebral hemorrhage (ICH) and a recent study indicates that CA-1 can cause blood-brain barrier disruption. The present study investigated the role of CA-1 in ICH-induced brain injury.There were three groups in the study. In the first, adult male Sprague-Dawley rats received 100 μl autologous blood injection into the right caudate. Sham rats had a needle insertion. Rat brains were used for brain CA-1 level determination. In the second group, rats received an intracaudate injection of either 50 μl CA-1 (1 μg/μl) or saline. Brain water content, microglia activation and neuronal death (Fluoro-Jade C staining) were examined 24 hours later. In the third group, acetazolamide (AZA, 5 μl, 1 mM), an inhibitor of carbonic anhydrases, or vehicle was co-injected with 100 μl blood. Brain water content, neuronal death and behavioral deficits were measured. We found that CA-I levels were elevated in the ipsilateral basal ganglia at 24 hours after ICH. Intracaudate injection of CA-1 induced brain edema (79.0 ± 0.6 vs. 78.0±0.2% in saline group, p<0.01), microglia activation and neuronal death (p<0.01) at 24 hours. AZA, an inhibitor of CA, reduced ICH-induced brain water content (79.3 ± 0.7 vs. 81.0 ± 1.0% in the vehicle-treated group, p<0.05), neuronal death and improved functional outcome (p<0.05).These results suggest that CA-1 from erythrocyte lysis contributes to brain injury after ICH.
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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.