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Updated: Nov 18, 2025
A Murine Model of Subarachnoid Hemorrhage
Published on: November 21, 2013
Correlation of cardiac function and cerebral perfusion in a murine model of subarachnoid hemorrhage
Axel Neulen1, Michael Molitor2,3,4, Michael Kosterhon5
1Department of Neurosurgery, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, 55131, Mainz, Germany. axel.neulen@unimedizin-mainz.de.
Insights
Subarachnoid hemorrhage (SAH) can cause cardiac issues, impacting brain blood flow. This study in mice shows heart function influences cerebral perfusion, suggesting left ventricular end-diastolic volume as a risk marker.
Area of Science:
- Neurology
- Cardiology
- Translational Medicine
Background:
- Cerebral hypoperfusion is critical after subarachnoid hemorrhage (SAH), affecting patient outcomes.
- Neurogenic stress cardiomyopathy (NSC) occurs in some SAH patients, but its impact on cerebral perfusion is not fully understood.
Purpose of the Study:
- To investigate the relationship between cardiac function and cerebral perfusion in a murine SAH model.
- To identify electrocardiographic (ECG) and echocardiographic markers of NSC post-SAH.
Main Methods:
- SAH was induced in mice using endovascular filament perforation.
- Cortical perfusion was measured using laser speckle contrast imaging.
- Myocardial function was assessed via serial high-frequency ultrasound and ECG.
Main Results:
- Cortical perfusion decreased post-SAH, while cardiac output and ejection fraction initially increased.
- Transient ECG and echocardiographic signs of NSC (e.g., right bundle branch block, reduced contractility) were observed within 3 hours.
- Cerebral perfusion recovery correlated with left ventricular end-diastolic volume (LVEDV) at multiple time points.
Conclusions:
- Cardiac dysfunction significantly influences cerebral perfusion following SAH, beyond cerebrovascular effects.
- The murine SAH model is suitable for studying NSC.
- LVEDV may serve as a valuable parameter for risk stratification in SAH patients with potential NSC.
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.
