System Analysis of Sympathetic Regulation of Heart Failure and Exploration of New Bionic Autonomic Neuromodulation Therapy

为了阐明交感神经调节在心力衰竭中的机制，我们检测了自发性高血压大鼠(SHR)的交感神经活动和血压对分离的颈动脉窦压力变化的反应，因为高血压被认为是心力衰竭的主要原因。与血压正常的Wistar京都大鼠(WKY)相比，神经弧(对颈动脉窦压力反应的交感神经活动)向更高的设定点移动，而周围弧(交感神经活动的升压反应)没有变化。自发性高血压大鼠的肾交感神经切断不仅通过压力感受性反射调节降低血压，而且通过将神经弧移向较低的设定点而独立地降低压力感受性反射。去肾神经的降压作用并不能使血压或交感神经活动完全恢复到WKY的水平。综上所述，神经调节治疗、去肾神经、降低交感神经活动，并通过交感神经活动的压力反射调节，降低了肾失神经SHR的血压。

To elucidate the mechanisms of sympathetic regulation in heart failure, we examined sympathetic nervous activity and blood pressure in response to change in isolated carotid sinus pressure in spontaneously hypertensive rats (SHR), as hypertension is considered the major cause of heart failure. The neural arc, the sympathetic nerve activity in response to carotid sinus pressure, shifted towards a higher set point whereas the peripheral arc, the pressor response to sympathetic nerve activity, did not change when compared with normotensive Wistar Kyoto Rats (WKY). Renal sympathetic nerve denervation in SHR reduced blood pressure not only through baroreflex regulation, but also baroreflex-independently by shifting the neural arc towards a lower set point. The antihypertensive effects of renal denervation did not completely normalize either blood pressure or sympathetic nervous activity to the levels seen in WKY. As a conclusion, the neuromodulation therapy, renal denervation, reduced sympathetic nervous activity, and, through the baroreflex regulation of sympathetic nervous activity, decreased blood pressure in renal denervated SHR compared to SHR.