Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-6316
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dc.contributor.authorNeulen, Axel-
dc.contributor.authorMolitor, Michael-
dc.contributor.authorKosterhon, Michael-
dc.contributor.authorPantel, Tobias-
dc.contributor.authorHolzbach, Elisa-
dc.contributor.authorRudi, Wolf-Stephan-
dc.contributor.authorKarbach, Susanne H.-
dc.contributor.authorWenzel, Philip-
dc.contributor.authorRingel, Florian-
dc.contributor.authorThal, Serge C.-
dc.date.accessioned2021-09-08T10:13:49Z-
dc.date.available2021-09-08T10:13:49Z-
dc.date.issued2021-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/6326-
dc.description.abstractCerebral hypoperfusion is a key factor for determining the outcome after subarachnoid hemorrhage (SAH). A subset of SAH patients develop neurogenic stress cardiomyopathy (NSC), but it is unclear to what extent cerebral hypoperfusion is influenced by cardiac dysfunction after SAH. The aims of this study were to examine the association between cardiac function and cerebral perfusion in a murine model of SAH and to identify electrocardiographic and echocardiographic signs indicative of NSC. We quantified cortical perfusion by laser SPECKLE contrast imaging, and myocardial function by serial high-frequency ultrasound imaging, for up to 7 days after experimental SAH induction in mice by endovascular filament perforation. Cortical perfusion decreased significantly whereas cardiac output and left ventricular ejection fraction increased significantly shortly post-SAH. Transient pathological ECG and echocardiographic abnormalities, indicating NSC (right bundle branch block, reduced left ventricular contractility), were observed up to 3 h post-SAH in a subset of model animals. Cerebral perfusion improved over time after SAH and correlated significantly with left ventricular end-diastolic volume at 3, 24, and 72 h. The murine SAH model is appropriate to experimentally investigate NSC. We conclude that in addition to cerebrovascular dysfunction, cardiac dysfunction may significantly influence cerebral perfusion, with LVEDV presenting a potential parameter for risk stratification.en_GB
dc.language.isoengde
dc.rightsCC BY*
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/*
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleCorrelation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhageen_GB
dc.typeZeitschriftenaufsatzde
dc.identifier.doihttp://doi.org/10.25358/openscience-6316-
jgu.type.dinitypearticleen_GB
jgu.type.versionPublished versionde
jgu.type.resourceTextde
jgu.organisation.departmentFB 04 Medizinde
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleScientific reportsde
jgu.journal.volume11de
jgu.pages.alternative3317de
jgu.publisher.year2021-
jgu.publisher.nameMacmillan Publishers Limited, part of Springer Naturede
jgu.publisher.placeLondonde
jgu.publisher.urihttps://doi.org/10.1038/s41598-021-82583-9de
jgu.publisher.issn2045-2322de
jgu.organisation.placeMainz-
jgu.subject.ddccode610de
jgu.publisher.doi10.1038/s41598-021-82583-9
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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