Malliani A, Pagani M
Eur Heart J. 1983 Jan;4 Suppl A:49-54. doi: 10.1093/eurheartj/4.suppl_a.49.
Congestive heart failure is usually accompanied by cardiovascular signs of an increased sympathetic and a decreased parasympathetic efferent activity. A current hypothesis for these autonomic changes holds the baroreceptor mechanisms mainly responsible for this complex neural reflex pattern together with a decreased responsiveness of cardiac vagal afferent ffibers. An alternative hypothesis is proposed here. Afferent sympathetic fibers with sensory endings in the atria and in the pulmonary veins are progressively excited by volume load. In cats with a chronic spinal section at C8, breathing spontaneously, an infusion of saline induces a reflex tachycardia through a sympatho-sympathetic neural circuit. In chronic dogs with intact cardiovascular innervation, the stimulation of aortic or cardiac sympathetic afferent fibers elicits an excitatory sympathetic reflex leading to hypertension and tachycardia; in addition, the sensitivity of baroreflexes is markedly reduced. Therefore, in congestive heart failure, especially in the absence of hypotension, the reflex excitation of the sympathetic outflow and the inhibition of the vagal efferent activity directed to the heart could be due to reflex mechanisms mediated by sympathetic cardiovascular afferents.
充血性心力衰竭通常伴有交感神经传出活动增强和副交感神经传出活动减弱的心血管体征。目前关于这些自主神经变化的一种假说认为,压力感受器机制主要负责这种复杂的神经反射模式,同时心脏迷走传入纤维的反应性降低。本文提出了另一种假说。心房和肺静脉中具有感觉末梢的交感传入纤维会因容量负荷而逐渐兴奋。在C8水平进行慢性脊髓横断、自主呼吸的猫中,输注生理盐水会通过交感-交感神经回路诱发反射性心动过速。在心血管神经支配完整的慢性犬中,刺激主动脉或心脏交感传入纤维会引发兴奋性交感反射,导致高血压和心动过速;此外,压力反射的敏感性会显著降低。因此,在充血性心力衰竭中,尤其是在无低血压的情况下,交感神经传出冲动的反射性兴奋以及对心脏迷走传出活动的抑制可能是由交感心血管传入介导的反射机制所致。