Emerging excitatory role of cardiovascular sympathetic afferents in pathophysiological conditions
Emerging excitatory role of cardiovascular sympathetic afferents in pathophysiological conditions
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DOI：
10.1161/hy0102.099200
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发表时间：
2002-01-01
期刊：
影响因子：
8.3
通讯作者：
Montano, N
中科院分区：
文献类型：
--
作者：
Malliani, A;Montano, N
有充分的实验证据表明，心血管交感传入纤维介导心血管反射，其本质上主要是兴奋性的，具有正反馈特征。这种传入神经通道很可能正常参与心血管功能的神经调节。本文的核心假设是，在某些病理生理条件下，交感神经过度活跃可能部分归因于心血管交感神经传入神经的兴奋性反射作用。事实上，充血性心力衰竭的早期阶段的特征是动脉压和心率增加和/或舒张功能障碍，而心输出量保持不变；在这些情况下，不应发生压力感受器失活，胸廓低压区具有感觉末梢的心血管交感神经传入，对容量负荷高度敏感，可能负责介导反射性交感神经兴奋。类似地，在急性心肌梗死期间，心室交感神经传入可能介导反射性交感神经过度活跃，已知这会促进猝死。最后，许多报告描述了原发性动脉高血压中交感神经活动的增加，这可能至少部分归因于交感交感反射的增强作用。因此，在病理生理条件下，心血管交感神经传入将介导独立于压力感受机制的反射性交感神经过度活动，并且这种稳态目的的缺失将为治疗校正的一些有益效果提供更好的理由。
There is sound experimental evidence that cardiovascular sympathetic afferent fibers mediate cardiovascular reflexes largely excitatory in nature with positive-feedback characteristics. This afferent neural channel is likely to normally participate in the neural regulation of cardiovascular function. The hypothesis, which is the core of this article, is that in some pathophysiological conditions, sympathetic overactivity may be partly due to an emerging excitatory reflex action of cardiovascular sympathetic afferents. In fact, the early phase of congestive heart failure can be characterized by an increase in arterial pressure and heart rate and/or by a diastolic dysfunction, leaving unchanged the cardiac output; in these conditions, in which no baroreceptor deactivation should occur, it is possible that cardiovascular sympathetic afferents with sensory endings in the thoracic low-pressure areas, highly responsive to volume loading, are responsible for mediating the reflex sympathetic excitation. Similarly, during acute myocardial infarction, ventricular sympathetic afferents are likely to mediate a reflex sympathetic overactivity, which is known to facilitate sudden death. Finally, numerous reports have described in essential arterial hypertension an increased sympathetic activity that may be due, at least in part, to the reinforcing action of sympathosympathetic reflexes. Thus, in pathophysiological conditions, cardiovascular sympathetic afferents would mediate a reflex sympathetic overactivity independently of baroreceptive mechanisms, and such an absence of a homeostatic purpose would provide a better rationale for some beneficial effects of therapeutic correction.