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Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-221
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dc.contributor.authorNeulen, Axel-
dc.contributor.authorPantel, Tobias-
dc.contributor.authorKosterhon, Michael-
dc.contributor.authorKramer, Andreas-
dc.contributor.authorKunath, Sascha-
dc.contributor.authorPetermeyer, Maximilian-
dc.contributor.authorMoosmann, Bernd-
dc.contributor.authorLotz, Johannes-
dc.contributor.authorKantelhardt, Sven Rainer-
dc.contributor.authorRingel, Florian-
dc.contributor.authorThal, Serge-
dc.date.accessioned2019-11-08T09:32:24Z-
dc.date.available2019-11-08T10:32:24Z-
dc.date.issued2019-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/223-
dc.description.abstractCerebral hypoperfusion in the first hours after subarachnoid haemorrhage (SAH) is a major determinant of poor neurological outcome. However, the underlying pathophysiology is only partly understood. Here we induced neutropenia in C57BL/6N mice by anti-Ly6G antibody injection, induced SAH by endovascular filament perforation, and analysed cerebral cortical perfusion with laser SPECKLE contrast imaging to investigate the role of neutrophils in mediating cerebral hypoperfusion during the first 24 h post-SAH. SAH induction significantly increased the intracranial pressure (ICP), and significantly reduced the cerebral perfusion pressure (CPP). At 3 h after SAH, ICP had returned to baseline and CPP was similar between SAH and sham mice. However, in SAH mice with normal neutrophil counts cortical hypoperfusion persisted. Conversely, despite similar CPP, cortical perfusion was significantly higher at 3 h after SAH in mice with neutropenia. The levels of 8-iso-prostaglandin-F2α in the subarachnoid haematoma increased significantly at 3 h after SAH in animals with normal neutrophil counts indicating oxidative stress, which was not the case in neutropenic SAH animals. These results suggest that neutrophils are important mediators of cortical hypoperfusion and oxidative stress early after SAH. Targeting neutrophil function and neutrophil-induced oxidative stress could be a promising new approach to mitigate cerebral hypoperfusion early after SAH.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleNeutrophils mediate early cerebral cortical hypoperfusion in a murine model of subarachnoid haemorrhageen_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.doihttp://doi.org/10.25358/openscience-221-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 04 Medizin-
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleScientific reports-
jgu.journal.volume9-
jgu.pages.alternativeArt. 8460-
jgu.publisher.year2019-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Nature-
jgu.publisher.placeLondon-
jgu.publisher.urihttp://dx.doi.org/10.1038/s41598-019-44906-9-
jgu.publisher.issn2045-2322-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2019-11-08T09:32:24Z-
opus.date.modified2019-11-14T09:52:46Z-
opus.date.available2019-11-08T10:32:24-
opus.subject.dfgcode04-205-
opus.organisation.stringFB 04: Medizin: Institut für Pathobiochemiede_DE
opus.organisation.stringFB 04: Medizin: Neurochirurgische Klinik und Poliklinikde_DE
opus.organisation.stringFB 04: Medizin: Institut für Klinische Chemie und Laboratoriumsmedizinde_DE
opus.organisation.stringFB 04: Medizin: Klinik für Anästhesiologiede_DE
opus.identifier.opusid59404-
opus.institute.number0473-
opus.institute.number0441-
opus.institute.number0428-
opus.institute.number0418-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_GB
opus.affiliatedNeulen, Axel-
opus.affiliatedKosterhon, Michael-
opus.affiliatedKunath, Sascha-
opus.affiliatedMoosmann, Bernd-
opus.affiliatedLotz, Johannes-
opus.affiliatedKantelhardt, Sven Rainer-
opus.affiliatedRingel, Florian-
opus.affiliatedThal, Serge-
jgu.publisher.doi10.1038/s41598-019-44906-9
jgu.organisation.rorhttps://ror.org/023b0x485
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