Abstract 57: Brain-heart Interaction: Age Aggravates Cardiac Damage After Cerebral Ischemic Stroke

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Zhili Chen ◽  
Tao Yan ◽  
Qiang Zhao ◽  
Yi Shen ◽  
Wei Li ◽  
...  

Background: The incidence of cardiovascular diseases is approximately three times higher in patients with neurological diseases than in patients without neurological diseases. Clinical findings have demonstrated that 70% of stroke patients exhibit cardiac dysfunction. Myocardial injury may occur after stroke in the absence of primary cardiac causes. In this study, we tested the hypothesis that age affects brain-heart interaction after cerebral ischemic stroke, and that aging increases cardiac dysfunction after stroke. Methods: Young adult (2-3 months), middle age (8-9 months) and aged (17-18 months) male C57BL mice were subjected to distal middle cerebral artery occlusion (dMCAo) or sham control (n=10/group). Cardiac hemodynamics and function were measured by transthoracic Doppler echocardiography. Mice were sacrificed at 28 days after surgery. Immunostaining of heart tissues were performed. To elucidate the mechanisms of stroke mediated cardiac dysfunction, heart tissue flow cytometry was employed to measure myocardial inflammation at 4 days after stroke in middle aged mice (n=6/group). Results: 1) Stroke mice exhibited an age dependent decrease in cardiac function: Stroke in young adult mice induced mild cardiac dysfunction; While the middle age and aged stroke mice exhibited significantly increased cardiac dysfunction compared to age matched sham controls, respectively (p<0.05). Middle age stroke mice exhibit significantly decreased ejection fraction (EF), and increased left ventricular systolic volume (LVVOLs) and LV volume during diastole (LVVOLd); Aged stroke mice exhibited significantly decreased EF and fractional shortening, increased LVVOLs LVVOLd, LV end-diastolic and end-systolic diameter, when compared to age matched sham controls, respectively. 2) Middle age and aged stroke mice exhibited significantly increased myocyte hypertrophy and fibrosis measured by Sirius red collagen staining. 3) Middle aged stroke mice exhibited significantly increased CD45 and CD11b high /CD45 + inflammation cell infiltration in the heart compared to middle age sham controls. Conclusion: Stroke induces cardiac dysfunction. Age affects brain-heart interaction, and age aggravates heart damage after cerebral ischemic stroke.

2021 ◽  
Vol Volume 14 ◽  
pp. 577-582
Author(s):  
Ali Alhashim ◽  
Mustafa Alqarni ◽  
Majed Alabdali ◽  
Mohammed Alshurem ◽  
Aishah Albakr ◽  
...  

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.


2015 ◽  
Vol 40 (9) ◽  
pp. 1786-1791 ◽  
Author(s):  
Lijuan Gu ◽  
Zhihong Jian ◽  
Creed Stary ◽  
Xiaoxing Xiong

2021 ◽  
Vol 15 ◽  
Author(s):  
Huiyong Liu ◽  
Sydney Reiter ◽  
Xiangyue Zhou ◽  
Hanmin Chen ◽  
Yibo Ou ◽  
...  

Strokes are the most common types of cerebrovascular disease and remain a major cause of death and disability worldwide. Cerebral ischemic stroke is caused by a reduction in blood flow to the brain. In this disease, two major zones of injury are identified: the lesion core, in which cells rapidly progress toward death, and the ischemic penumbra (surrounding the lesion core), which is defined as hypoperfusion tissue where cells may remain viable and can be repaired. Two methods that are approved by the Food and Drug Administration (FDA) include intravenous thrombolytic therapy and endovascular thrombectomy, however, the narrow therapeutic window poses a limitation, and therefore a low percentage of stroke patients actually receive these treatments. Developments in stem cell therapy have introduced renewed hope to patients with ischemic stroke due to its potential effect for reversing the neurological sequelae. Over the last few decades, animal tests and clinical trials have been used to treat ischemic stroke experimentally with various types of stem cells. However, several technical and ethical challenges must be overcome before stem cells can become a choice for the treatment of stroke. In this review, we summarize the mechanisms, processes, and challenges of using stem cells in stroke treatment. We also discuss new developing trends in this field.


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