Xu Bin, Li Hongli
Department of Cardiology, Shanghai First People's Hospital, College of Medicine, Shanghai Jiaotong University, Shanghai 200080, P.R. China.
Mol Med Rep. 2015 Dec;12(6):7823-9. doi: 10.3892/mmr.2015.4434. Epub 2015 Oct 13.
Patients with chronic heart failure (CHF) have an insufficient perfusion to the peripheral tissues due to decreased cardiac output. The compensatory mechanisms are triggered even prior to the occurrence of clinical symptoms, which include activation of the sympathetic nervous system (SNS) and other neurohumoral factors. However, the long‑term activation of the SNS contributes to progressive cardiac dysfunction and has toxic effects on the cardiomyocytes. The mechanisms leading to the activation of SNS include changes in peripheral baroreceptor and chemoreceptor reflexes and the abnormal regulation of sympathetic nerve activity (SNA) in the central nervous system (CNS). Recent studies have focused on the role of brain mechanisms in the regulation of SNA and the progression of CHF. The renin‑angiotensin system, nitric oxide and pro‑inflammatory cytokines were shown to be involved in the abnormal regulation of SNA in the CNS. The alteration of these neurohumoral factors during CHF influences the activity of neurons in the autonomic regions and finally increase the sympathetic outflow. The present review summarizes the brain mechanisms contributing to sympathoexcitation in CHF.
慢性心力衰竭（CHF）患者由于心输出量降低，外周组织灌注不足。甚至在临床症状出现之前，代偿机制就已被触发，其中包括交感神经系统（SNS）和其他神经体液因子的激活。然而，SNS的长期激活会导致进行性心脏功能障碍，并对心肌细胞产生毒性作用。导致SNS激活的机制包括外周压力感受器和化学感受器反射的变化以及中枢神经系统（CNS）中交感神经活动（SNA）的异常调节。最近的研究集中在脑机制在SNA调节和CHF进展中的作用。肾素-血管紧张素系统、一氧化氮和促炎细胞因子被证明参与了CNS中SNA的异常调节。CHF期间这些神经体液因子的改变会影响自主神经区域神经元的活动，最终增加交感神经输出。本综述总结了导致CHF交感神经兴奋的脑机制。
