心力衰竭时血浆中正肾上腺素水平升高,是由于中枢性交感神经向肌肉的传递增加,神经活力的程度与心脏损害的严重性呈负相关。中枢性传出交感神经活性增加的病因有待进一步明确。动物实验模型提示,心肺和动脉压力反射机制的损害,是病因的重要环节。在人类,心力衰竭伴有控制心率、血管阻力和血浆正肾上腺素的压力反射的损害。本文研究是应用经皮、腓骨侧的微神经图,直接测定正常人和心衰病人的交感神经活性,以验证临床心衰时传出交感神经传递的压力反射控制受到损害这一假设。 Heart failure plasma norepinephrine levels, due to increased transmission of the central sympathetic to the muscle, the degree of nerve activity and the severity of cardiac damage was negatively correlated. The etiology of increased sympathetic activity in the central nervous system needs to be further clarified. Animal models suggest that impairment of cardiopulmonary and arterial pressure reflex mechanisms is an important part of the cause. In humans, heart failure is accompanied by the control of heart rate, vascular resistance, and plasma pressure-norepinephrine reflex damage. This study is based on the percutaneous, fibular side of the micro-neurogram, direct determination of normal and heart failure in patients with sympathetic nerve activity in order to verify the clinical outbreak of sympathetic nerve afferent neurotransmission stress reflex control hypothesis.