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  1. Article: Neuroprotection by inhaled nitric oxide in a murine stroke model is concentration and duration dependent

    Li, Yong-Sheng / Shemmer, Benjamin / Stone, Eric / A Nardi, Michael / Jonas, Saran / Quartermain, David

    Brain research. 2013 Apr. 24, v. 1507

    2013  

    Abstract: Inhaled nitric oxide (iNO) has been shown to reduce ischemia/reperfusion (I/R) injury in several different organ systems including the brain. We investigated whether iNO was neuroprotective in a mouse model of transient focal ischemia. Male Swiss Webster ...

    Abstract Inhaled nitric oxide (iNO) has been shown to reduce ischemia/reperfusion (I/R) injury in several different organ systems including the brain. We investigated whether iNO was neuroprotective in a mouse model of transient focal ischemia. Male Swiss Webster mice underwent middle cerebral artery occlusion for 1h followed by reperfusion for 47h. Mice were divided into 5 concentration groups and administered nitric oxide (NO) at either 10, 20, 40, 60 or 80ppm. Each of the 5 concentration groups was subdivided into 4 duration groups which were treated with iNO for 5, 8, 16 or 24h beginning immediately after artery occlusion. Results showed both concentration and duration determined efficacy. At 10ppm only the 24hr duration group exhibited reduced infarct volume while at 20, 40 and 60ppm only 8 and 16h of exposure led to smaller infarctions. At these concentrations the dose response curves were strongly U shaped indicating a loss of benefit at long durations. At 80ppm, reduction in infarct volume was not observed at any duration. Additional experiments showed that 60ppm iNO could be transported from lung to brain and that iNO administered for 8h improved recovery from subarachnoid hemorrhage and reduced the inflammatory response accompanying ischemic stroke. Enhanced blood flow during reperfusion may be an important mediator of these effects.
    Keywords animal models ; blood flow ; brain ; dose response ; hemorrhage ; infarction ; inflammation ; ischemia ; mice ; neuroprotective effect ; nitric oxide ; stroke
    Language English
    Dates of publication 2013-0424
    Size p. 134-145.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2013.02.031
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  2. Article ; Online: Neuroprotection by inhaled nitric oxide in a murine stroke model is concentration and duration dependent.

    Li, Yong-Sheng / Shemmer, Benjamin / Stone, Eric / A Nardi, Michael / Jonas, Saran / Quartermain, David

    Brain research

    2013  Volume 1507, Page(s) 134–145

    Abstract: Inhaled nitric oxide (iNO) has been shown to reduce ischemia/reperfusion (I/R) injury in several different organ systems including the brain. We investigated whether iNO was neuroprotective in a mouse model of transient focal ischemia. Male Swiss Webster ...

    Abstract Inhaled nitric oxide (iNO) has been shown to reduce ischemia/reperfusion (I/R) injury in several different organ systems including the brain. We investigated whether iNO was neuroprotective in a mouse model of transient focal ischemia. Male Swiss Webster mice underwent middle cerebral artery occlusion for 1 h followed by reperfusion for 47 h. Mice were divided into 5 concentration groups and administered nitric oxide (NO) at either 10, 20, 40, 60 or 80 ppm. Each of the 5 concentration groups was subdivided into 4 duration groups which were treated with iNO for 5, 8, 16 or 24 h beginning immediately after artery occlusion. Results showed both concentration and duration determined efficacy. At 10 ppm only the 24hr duration group exhibited reduced infarct volume while at 20, 40 and 60 ppm only 8 and 16 h of exposure led to smaller infarctions. At these concentrations the dose response curves were strongly U shaped indicating a loss of benefit at long durations. At 80 ppm, reduction in infarct volume was not observed at any duration. Additional experiments showed that 60 ppm iNO could be transported from lung to brain and that iNO administered for 8h improved recovery from subarachnoid hemorrhage and reduced the inflammatory response accompanying ischemic stroke. Enhanced blood flow during reperfusion may be an important mediator of these effects.
    MeSH term(s) Administration, Inhalation ; Animals ; Brain/blood supply ; Brain/drug effects ; Disease Models, Animal ; Infarction, Middle Cerebral Artery/drug therapy ; Male ; Mice ; Neuroprotective Agents/administration & dosage ; Neuroprotective Agents/therapeutic use ; Nitric Oxide/administration & dosage ; Nitric Oxide/therapeutic use ; Reperfusion Injury/drug therapy ; Stroke/drug therapy
    Chemical Substances Neuroprotective Agents ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2013-04-24
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2013.02.031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 161: Show issues Location:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  3. Article: Neuroprotection by inhaled nitric oxide in a murine stroke model is concentration and duration dependent

    Li, Yong-Sheng / Shemmer, Benjamin / Stone, Eric / A Nardi, Michael / Jonas, Saran / Quartermain, David

    Brain research

    Volume v. 1507

    Abstract: Inhaled nitric oxide (iNO) has been shown to reduce ischemia/reperfusion (I/R) injury in several different organ systems including the brain. We investigated whether iNO was neuroprotective in a mouse model of transient focal ischemia. Male Swiss Webster ...

    Abstract Inhaled nitric oxide (iNO) has been shown to reduce ischemia/reperfusion (I/R) injury in several different organ systems including the brain. We investigated whether iNO was neuroprotective in a mouse model of transient focal ischemia. Male Swiss Webster mice underwent middle cerebral artery occlusion for 1h followed by reperfusion for 47h. Mice were divided into 5 concentration groups and administered nitric oxide (NO) at either 10, 20, 40, 60 or 80ppm. Each of the 5 concentration groups was subdivided into 4 duration groups which were treated with iNO for 5, 8, 16 or 24h beginning immediately after artery occlusion. Results showed both concentration and duration determined efficacy. At 10ppm only the 24hr duration group exhibited reduced infarct volume while at 20, 40 and 60ppm only 8 and 16h of exposure led to smaller infarctions. At these concentrations the dose response curves were strongly U shaped indicating a loss of benefit at long durations. At 80ppm, reduction in infarct volume was not observed at any duration. Additional experiments showed that 60ppm iNO could be transported from lung to brain and that iNO administered for 8h improved recovery from subarachnoid hemorrhage and reduced the inflammatory response accompanying ischemic stroke. Enhanced blood flow during reperfusion may be an important mediator of these effects.
    Keywords mice ; stroke ; inflammation ; infarction ; dose response ; nitric oxide ; neuroprotective effect ; blood flow ; ischemia ; animal models ; brain ; hemorrhage
    Language English
    Document type Article
    ISSN 0006-8993
    Database AGRIS - International Information System for the Agricultural Sciences and Technology

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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