Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage

Abstract Cerebral 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 o...

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Autores principales:	Axel Neulen, Michael Molitor, Michael Kosterhon, Tobias Pantel, Elisa Holzbach, Wolf-Stephan Rudi, Susanne H. Karbach, Philip Wenzel, Florian Ringel, Serge C. Thal
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e1369802973a4cc987503f1fda9444ff
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spelling	oai:doaj.org-article:e1369802973a4cc987503f1fda9444ff2021-12-02T14:26:48ZCorrelation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage10.1038/s41598-021-82583-92045-2322https://doaj.org/article/e1369802973a4cc987503f1fda9444ff2021-02-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-82583-9https://doaj.org/toc/2045-2322Abstract Cerebral 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.Axel NeulenMichael MolitorMichael KosterhonTobias PantelElisa HolzbachWolf-Stephan RudiSusanne H. KarbachPhilip WenzelFlorian RingelSerge C. ThalNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Axel Neulen Michael Molitor Michael Kosterhon Tobias Pantel Elisa Holzbach Wolf-Stephan Rudi Susanne H. Karbach Philip Wenzel Florian Ringel Serge C. Thal Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
description	Abstract Cerebral 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.
format	article
author	Axel Neulen Michael Molitor Michael Kosterhon Tobias Pantel Elisa Holzbach Wolf-Stephan Rudi Susanne H. Karbach Philip Wenzel Florian Ringel Serge C. Thal
author_facet	Axel Neulen Michael Molitor Michael Kosterhon Tobias Pantel Elisa Holzbach Wolf-Stephan Rudi Susanne H. Karbach Philip Wenzel Florian Ringel Serge C. Thal
author_sort	Axel Neulen
title	Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
title_short	Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
title_full	Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
title_fullStr	Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
title_full_unstemmed	Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
title_sort	correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/e1369802973a4cc987503f1fda9444ff
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Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage

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