ArticlePloS one2017
Therapeutic time window for conivaptan treatment against stroke-evoked brain edema and blood-brain barrier disruption in mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The neuropeptide in ischemic brain injury: insights, challenges, and horizon of targeted interventions.Journal of translational medicine · 2026Pooled it
- The dual role of arginine vasopressin in immune regulation: Balancing immunostimulation and immunosuppression.Brain, behavior, & immunity - health · 2026Review
- The Role of Arginine-Vasopressin in Stroke and the Potential Use of Arginine-Vasopressin Type 1 Receptor Antagonists in Stroke Therapy: A Narrative Review.International journal of molecular sciences · 2023Review
- Imaging Acute Stroke: From One-Size-Fit-All to Biomarkers.Frontiers in neurology · 2021Review
- Triblock Copolymer Nanomicelles Loaded with Curcumin Attenuates Inflammation via Inhibiting the NF-κB Pathway in the Rat Model of Cerebral Ischemia.International journal of nanomedicine · 2021Article
- Bioinformatics Identification of Ferroptosis-Related Biomarkers and Therapeutic Compounds in Ischemic Stroke.Frontiers in neurology · 2021Article
- Potential Therapies for Cerebral Edema After Ischemic Stroke: A Mini Review.Frontiers in aging neuroscience · 2020Review
- Article
- Disrupting interaction of PSD-95 with nNOS attenuates hemorrhage-induced thalamic pain.Neuropharmacology · 2018Article
- The role of nitric oxide in stroke.Medical gas researchReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIschemic stroke is often complicated by brain edema, disruption of blood-brain barrier (BBB), and uncontrolled release of arginine-vasopressin (AVP). Conivaptan, a V1a and V2 receptor antagonist, reduces brain edema and minimizes damage to the blood-brain barrier after stroke. Most stroke patients do not receive treatment immediately after the onset of brain ischemia. Delays in therapy initiation may worsen stroke outcomes. Therefore, we designed a translational study to explore the therapeutic time window for conivaptan administration.
methodsMice were treated with conivaptan beginning 3, 5, or 20 hours after 60-minute focal middle cerebral artery occlusion. Treatments were administered by continuous IV infusion for a total of 48 hours. Brain edema and blood-brain barrier (BBB) disruption were evaluated at endpoint.
resultsConivaptan therapy initiated at 3 hours following ischemia reduced edema in the ipsilateral hemisphere, which corresponded with improvements in neurological deficits. Stroke-triggered BBB disruption was also reduced in mice when conivaptan treatments were initiated at 3 hours of reperfusion. However, 5 and 20-hour delays of conivaptan administration failed to reduce edema or protect BBB.
conclusionTiming of conivaptan administration is important for successful reduction of brain edema and BBB disruption. Our experimental data open new possibilities to repurpose conivaptan, and make an important "bench-to-bedside translation" of the results into clinical practice.
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