Immune response mediates brain-heart interaction after subarachnoid hemorrhage

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Conference Proceeding

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Background: Cardiac dysfunction is evident after Subarachnoid Hemorrhage (SAH). Patients with cardiovascular complications after SAH have 3.5 times increased risk of death compared with non-cardiac complication SAH patients. The immune system may contribute to the cardiac pathological processes post-SAH.This study investigates the possible role of the immune system in mediating cardiac dysfunction after SAH in mice. Methods: Adult male C57BL/6J mice were subjected to SAH model or sham-control. The experimental groups includes (n=15/group): 1) Sham-control; 2) SAH alone; 3) SAH+splenectomy (SAH+SP). Splenectomy was performed one week before SAH. Cardiac hemodynamics and function were measured by echocardiography at 3 days after SAH. The Garcia behavior score was performed . Mice were sacrificed at the third day after SAH. Cardiac tissue immunostaining (n=10/group) and flow cytometry (n=5/group) were performed. Results: We found that: 1) SAH alone induces significant neurological deficit and vasospasm compared to sham-control. SAH+SP significantly decrease neurological deficit, but no significant improvement in the vasospasm compared to SAH mice (p<0.05). 2) SAH mice exhibit significant cardiac dysfunction identified by a decline cardiac ejection fractions (EF) and fraction shortening (FS) compared to the sham. SAH+SP significantly improves cardiac function by increasing EF and FS compared to SAH mice (P<0.05). 3) SAH significantly increases inflammatory cells (CD11b+/CD45+/F480+ macrophages) infiltration into the heart compared to sham-control (p<0.05). The amount of macrophages within the heart tissue was significantly decreased in SAH+SP group when compared with the SAH group. 4) MCP1 expression in the heart was significantly increased in SAH group compared to sham; SAH+SP significantly decreased MCP1 expression compared to SAH (p<0.05). Conclusions: SAH induces cardiac dysfunction; SAH with splenectomy decreases heart inflammatory cell infiltration, inflammatory factor expression as well as decreases cardiac dysfunction after SAH. Immune response may play an important role in SAH-induced cardiac dysfunction.




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