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10.1371/journal.pone.0183985 http://scihub22266oqcxt.onion/10.1371/journal.pone.0183985 C5576654!5576654 !28854286     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28854286 &cmd=llinks): Failed to open stream: HTTP request failed! 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Therapeutic time window for conivaptan treatment against stroke-evoked brain edema and blood-brain barrier disruption in mice |pdf=|usr=}}{{28854286 }} gab.com Text Therapeutic time window for conivaptan treatment against stroke-evoked brain edema and blood-brain barrier disruption in mice JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28854286 #FOAvip BACKGROUND: Ischemic 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. METHODS: Mice 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. RESULTS: Conivaptan 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. CONCLUSION: Timing 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. Twit Text FOAVip Therapeutic time window for conivaptan treatment against stroke-evoked brain edema and blood-brain barrier disruption in mice ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28854286 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28854286 #FOAvip English Wikipedia <ref>{{Cite pmid|28854286 }}</ref> Therapeutic time window for conivaptan treatment against stroke-evoked brain edema and blood-brain barrier disruption in mice #MMPMID28854286 Zeynalov E ; Jones SM ; Elliott JP PLoS One 2017[]; 12 (8 ): e0183985 PMID28854286 show ga BACKGROUND: Ischemic 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. METHODS: Mice 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. RESULTS: Conivaptan 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. CONCLUSION: Timing 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. |Animals [MESH] |Antidiuretic Hormone Receptor Antagonists/*therapeutic use [MESH] |Benzazepines/*therapeutic use [MESH] |Blood-Brain Barrier/*drug effects/pathology [MESH] |Brain Edema/*drug therapy/*etiology/pathology [MESH] |Infarction, Middle Cerebral Artery/*complications/pathology [MESH] |Male [MESH] |Mice [MESH]Therapeutic time window for conivaptan treatment against stroke-evoked(epmc).pdf DeepDyve Pubget Overpricing