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

为了阐明心力衰竭的交感神经调节机制，我们研究了自发性高血压大鼠（SHR）的交感神经活动和血压对孤立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（交感神经活动对颈动脉窦压力的反应）向更高的设定点移动，而外周弧（交感神经活动的升压反应）没有变化。SHR去肾交感神经不仅通过压力反射调节血压，而且通过将神经弧移向较低的设定点而非压力反射依赖地降低血压。去肾神经的抗高血压作用并没有使血压或交感神经活动完全恢复到WKY的水平。总之，与SHR相比，去肾神经SHR的神经调节治疗，去肾神经，减少交感神经活动，并且通过交感神经活动的压力反射调节，降低血压。

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.