The high rates of mortality and disability resulting from intracerebral hemorrhage (ICH) are closely related to subsequent cardiac complications. The mechanisms underlying ICH-induced cardiac dysfunction are not fully understood. In this study, we investigated the role of sympathetic overactivity in mediating cardiac dysfunction post ICH in mice. Collagenase-injection ICH model was established in adult male C57BL/6J mice. Neurological function was subsequently evaluated at multiple time points after ICH and cardiac function was measured by echocardiography on 3 and 14 days after ICH. Plasma adrenaline, noradrenaline, cortisol and heart β1 adrenergic receptor (β1-AR) levels were assessed to evaluate sympathetic activity. Picro Sirius Red (PSR) staining was performed to evaluate cardiomyocyte hypertrophy and interstitial fibrosis. Monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interleukin-6(IL-6), nuclear factor kappa-B(NF-κB), NADPH oxidase-2 (NOX2), matrix metalloprotein (MMP-9) and transforming growth factor-beta (TGF-β) levels were assessed to evaluate inflammation, fibrosis and oxidative stress levels in heart after ICH. Macrophages and neutrophils were assessed to evaluate inflammatory cell infiltration in heart after ICH. ICH induced sympathetic excitability, as identified by increased circulating adrenaline, noradrenaline, cortisol levels and β1-AR expression in heart tissue. Metoprolol-treated ICH mice had improved cardiac and neurological function. The suppression of sympathetic overactivity by metoprolol attenuates cardiac inflammation, fibrosis and oxidative stress after ICH. In conclusion, ICH-induced secondary sympathetic overactivity which mediated inflammatory response may play an important role in post-ICH cardiac dysfunction.

脑出血 (ICH) 导致的高死亡率和致残率与随后的心脏并发症密切相关。ICH 引起的心脏功能障碍的潜在机制尚不完全清楚。在这项研究中，我们调查了交感神经过度活跃在介导 ICH 后小鼠心脏功能障碍中的作用。在成年雄性 C57BL/6J 小鼠中建立胶原酶注射 ICH 模型。随后在 ICH 后的多个时间点评估神经功能，并在 ICH 后 3 天和 14 天通过超声心动图测量心脏功能。评估血浆肾上腺素、去甲肾上腺素、皮质醇和心脏 β1 肾上腺素能受体 (β1-AR) 水平以评估交感神经活动。进行 Picro Sirius Red (PSR) 染色以评估心肌细胞肥大和间质纤维化。单核细胞趋化蛋白 1 (MCP-1)、肿瘤坏死因子-α (TNF-α)、白细胞介素-6(IL-6)、核因子 kappa-B(NF-κB)、NADPH 氧化酶-2 (NOX2)、基质评估金属蛋白 (MMP-9) 和转化生长因子-β (TGF-β) 水平以评估 ICH 后心脏的炎症、纤维化和氧化应激水平。评估巨噬细胞和中性粒细胞以评估 ICH 后心脏中的炎症细胞浸润。ICH 诱导交感神经兴奋性，如心脏组织中循环肾上腺素、去甲肾上腺素、皮质醇水平和 β1-AR 表达增加所确定的。美托洛尔治疗的 ICH 小鼠的心脏和神经功能得到改善。美托洛尔抑制交感神经过度活动可减轻 ICH 后的心脏炎症、纤维化和氧化应激。综上所述，