CLINICAL ASPECTS OF SYMPATHETIC ACTIVATION AND PARASYMPATHETIC WITHDRAWAL IN HEART-FAILURE
CLINICAL ASPECTS OF SYMPATHETIC ACTIVATION AND PARASYMPATHETIC WITHDRAWAL IN HEART-FAILURE
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DOI：
10.1016/0735-1097(93)90466-e
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发表时间：
1993-10-01
影响因子：
24
通讯作者：
FLORAS, JS
中科院分区：
文献类型：
--
作者：
FLORAS, JS
提出的心力衰竭全身神经体液激活的反射机制包括来自抑制性压力感受器传入血管的输入减少和来自动脉化学感受器、骨骼肌代谢感受器或肺的兴奋性传入血管的输入增加。并非所有左心室功能障碍的受试者都具有增加的交感神经活性，但交感神经激活的幅度似乎独立地预测存活。这种关联表明交感神经激活与不良结果之间的因果关系，以及通过抑制中枢交感神经流出来改善此类患者预后的治疗机会。肝硬化和衰老，不共享充血性心力衰竭的暗淡预后。肾上腺素能激活对患病心肌的不良影响可能是心脏交感神经活动增加的幅度和时间过程的函数，衰竭心脏中交感神经支配的不均匀异常的机械和电生理后果，以及在也以交感神经交通增加为特征的其他疾病中存在的特定抵消机制的缺乏。尚未专门验证以下假设：激活对病变心肌的肾上腺素能驱动是交感神经兴奋与不良结局相关的致病机制，以及抑制交感神经流出心脏的干预措施将改善充血性心力衰竭患者的预后。更好地理解的机制，负责响应心室功能障碍的交感神经激活的异质性，心脏特异性和全身性的交感神经系统的激活和刺激或抑制的抵消机制能够抵抗其不利影响是根本的发展更好的治疗充血性心力衰竭。
Proposed reflex mechanisms for generalized neurohumoral activation in heart failure include decreased input from inhibitory baroreceptor afferent vessels and increased input from excitatory afferent vessels arising from arterial chemoreceptors, skeletal muscle metaboreceptors or the lungs, Not all subjects with left ventricular dysfunction have increased sympathetic nerve activity, but the magnitude of sympathoneural activation appears to independently predict survival. This association suggests both a causative mechanism linking sympathetic activation with adverse outcome and a therapeutic opportunity to improve the prognosis of such patients by inhibiting central sympathetic outflow.Generalized sympathetic activation is not unique to heart failure, and its functional consequences appear to be both organ- and condition-specific, Sympathetic activation is present in other disorders such as mild hypertension, cirrhosis and aging that do not share the dim prognosis of congestive heart failure. The adverse effects of adrenergic activation on the diseased myocardium may be a function of the magnitude and time course of increases in cardiac sympathetic nerve activity, the mechanical and electrophysiologic consequences of nonuniform abnormalities of sympathetic innervation in the failing heart and the absence of specific countervailing mechanisms present in other conditions also characterized by increased sympathetic traffic. The hypotheses that activation of adrenergic drive to the diseased myocardium is the causative mechanism linking sympathoexcitation to adverse outcome and that interventions that inhibit sympathetic outflow to the heart will improve the prognosis of patients with congestive heart failure have not been specifically tested. Greater understanding of the mechanisms responsible for the heterogeneity of sympathetic activation in response to ventricular dysfunction, for cardiac-specific and generalized activation of the sympathetic nervous system and for the stimulation or suppression of countervailing mechanisms capable of resisting its adverse effects is fundamental to the development of better therapies for congestive heart failure.