A novel murine model of subarachnoid hemorrhage was developed to explore how catecholamine release and parasympathetic dysfunction may allow unchecked inflammation leading to myocardial damage.
Highlights the potential role of inflammation driven by autonomic dysfunction in mediating heart damage following subarachnoid hemorrhage.
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.
Mashaly et al. (Sat,) conducted a review in Subarachnoid hemorrhage. A novel murine model of subarachnoid hemorrhage was developed to explore how catecholamine release and parasympathetic dysfunction may allow unchecked inflammation leading to myocardial damage.
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