Related Experiment Video
Updated: Jul 4, 2026

Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging (MRI)
Published on: December 16, 2021
Inflammation as a link between brain injury and heart damage: the model of subarachnoid hemorrhage
Hazem Antar Mashaly1, J Javier Provencio
1Neuroinflammation Research Center, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
Insights
Subarachnoid hemorrhage (SAH) can cause heart problems due to inflammation. Researchers developed a new mouse model to study how SAH impacts the heart and leads to cell death.
Area of Science:
- Cardiology
- Neurology
- Pathophysiology
Background:
- Subarachnoid hemorrhage (SAH) is a model for studying heart-brain interactions.
- SAH is linked to high rates of arrhythmia but low coronary heart disease prevalence.
- The exact cause of cardiac issues in SAH remains unclear.
Purpose of the Study:
- To investigate the inflammatory mechanisms underlying cardiac damage in SAH.
- To explore the role of catecholamine release and parasympathetic dysfunction in SAH-induced myocardial injury.
Main Methods:
- Development of a novel murine model of subarachnoid hemorrhage.
- Utilizing this model to study heart-brain interactions and cardiac pathology.
Main Results:
- The study established a new SAH model in mice.
- This model allows for the investigation of cardiac dysfunction following SAH.
Conclusions:
- Inflammation, driven by catecholamine release and parasympathetic dysfunction, may cause myocardial dysfunction and cell death in SAH.
- The novel murine model provides a platform for further research into SAH-related cardiac complications.
Abstract:
Subarachnoid hemorrhage (SAH) serves as a good model for the study of heart-brain interactions because it is associated with both a high incidence of arrhythmia and a low prevalence of coronary heart disease. The pathophysiology of cardiac abnormalities in SAH is unsettled. Initial theories focused on sustained stimulation of cardiomyocytes at sympathetic nerve endings, but recent data suggest that dysfunction of the parasympathetic nervous system may contribute as well. We believe that the coupling of catecholamine release with parasympathetic dysfunction may allow unchecked inflammation that leads to myocardial dysfunction and cell death. We have developed a novel murine model of SAH to explore these potential inflammatory underpinnings of cardiac damage in SAH.
Related Concept Videos
Hemorrhagic Stroke ll: Pathophysiology
Hemorrhagic Stroke l: Introduction
Bacterial Meningitis II: Pathophysiology
Ischemic Stroke ll: Pathophysiology

