Central mechanisms of abnormal sympathoexcitation in chronic heart failure.
Central mechanisms of abnormal sympathoexcitation in chronic heart failure.
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DOI：
10.1155/2012/847172
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发表时间：
2012
影响因子：
2.1
通讯作者：
Hirooka Y
中科院分区：
文献类型：
--
作者：
Kishi T;Hirooka Y
已经认识到，交感神经系统在慢性心力衰竭中被异常激活，并导致慢性心力衰竭进一步恶化。在慢性心力衰竭的治疗中，许多临床研究已经表明，β受体阻滞剂对异常交感神经亢进的抑制是有益的。传统观点认为慢性心力衰竭时交感神经异常亢进是由兴奋性输入增强引起的，包括外周压力感受性反射和化学感受性反射以及控制交感神经流出的化学介质的变化。近年来，脑内肾素-血管紧张素系统-氧化应激轴和/或促炎细胞因子介导的交感神经活动中枢调节异常受到关注。中枢肾素血管紧张素系统、促炎细胞因子及其相互作用已被确定为慢性心力衰竭实验动物模型中交感神经抑制治疗的靶点。总之，我们必须认识到，慢性心力衰竭是一种异常的交感兴奋综合征，这是由交感神经活动的中枢调节异常引起的。
It has been recognized that the sympathetic nervous system is abnormally activated in chronic heart failure, and leads to further worsening chronic heart failure. In the treatment of chronic heart failure many clinical studies have already suggested that the inhibition of the abnormal sympathetic hyperactivity by beta blockers is beneficial. It has been classically considered that abnormal sympathetic hyperactivity in chronic heart failure is caused by the enhancement of excitatory inputs including changes in peripheral baroreceptor and chemoreceptor reflexes and chemical mediators that control sympathetic outflow. Recently, the abnormalities in the central regulation of sympathetic nerve activity mediated by brain renin angiotensin system-oxidative stress axis and/or proinflammatory cytokines have been focused. Central renin angiotensin system, proinflammatory cytokines, and the interaction between them have been determined as the target of the sympathoinhibitory treatment in experimental animal models with chronic heart failure. In conclusion, we must recognize that chronic heart failure is a syndrome with an abnormal sympathoexcitation, which is caused by the abnormalities in the central regulation of sympathetic nerve activity.