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Published on: May 15, 2019
Stress worsens endothelial function and ischemic stroke via glucocorticoids
Mustafa Balkaya1, Vincent Prinz, Florian Custodis
1Klinik für Neurologie, Charité-Universitätsmedizin Berlin, Chariteplatz 1, Berlin, Germany 10117.
Chronic stress worsens stroke outcomes by impairing blood vessel function. Blocking the stress hormone receptor with mifepristone reversed these harmful effects, reducing brain injury in mice.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Endocrinology
Background:
- Chronic stress is a known risk factor for stroke.
- The precise mechanisms linking stress to stroke remain unclear.
- This study investigates stress's impact on endothelial function and brain injury.
Purpose of the Study:
- To determine the effects of chronic stress on endothelial function.
- To assess the impact of chronic stress on ischemic brain injury.
- To evaluate the therapeutic potential of a glucocorticoid receptor antagonist.
Main Methods:
- Mice underwent 28 days of chronic stress, with some receiving mifepristone.
- Physiological parameters, endothelial function markers, and oxidative stress were measured.
- Ischemic brain lesion volume was quantified after middle cerebral artery occlusion.
Main Results:
- Chronic stress elevated heart rate, impaired vasodilation, and increased oxidative stress.
- Endothelial nitric oxide synthase levels decreased in stressed mice.
- Stressed mice exhibited larger ischemic brain lesion volumes, which were reduced by mifepristone.
Conclusions:
- Chronic stress exacerbates stroke vulnerability via endothelial dysfunction.
- Glucocorticoid receptor antagonism can mitigate stress-induced endothelial dysfunction and brain injury.
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