Malliani Alberto, Montano Nicola
Istituto di Scienze Biomediche, DiSP LITA di Vialba, Ospedale L. Sacco, Università di Milano, Milano, Italy.
Hypertension. 2002 Jan;39(1):63-8. doi: 10.1161/hy0102.099200.
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.
有可靠的实验证据表明，心血管交感传入纤维介导的心血管反射在本质上主要是兴奋性的，具有正反馈特征。这条传入神经通道可能正常参与心血管功能的神经调节。本文的核心假设是，在某些病理生理状况下，交感神经活动亢进可能部分归因于心血管交感传入神经新出现的兴奋性反射作用。事实上，充血性心力衰竭的早期阶段可表现为动脉压和心率升高及/或舒张功能障碍，而心输出量不变；在这些不应发生压力感受器失活的情况下，位于胸段低压区、对容量负荷高度敏感的心血管交感传入神经可能介导了反射性交感神经兴奋。同样，在急性心肌梗死期间，心室交感传入神经可能介导反射性交感神经活动亢进，而这已知会促使猝死。最后，众多报告描述了原发性高血压中交感神经活动增强，这可能至少部分归因于交感神经反射的增强作用。因此，在病理生理状况下，心血管交感传入神经会独立于压力感受机制介导反射性交感神经活动亢进，而这种缺乏稳态目的的情况将为治疗纠正的一些有益效果提供更好的理论依据。
