Division of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, Case Western Reserve University, Cleveland, OH 44106-5067, USA.
Respir Physiol Neurobiol. 2010 Nov 30;174(1-2):135-45. doi: 10.1016/j.resp.2010.09.006. Epub 2010 Sep 15.
Sympathetic nerve activity (SNA) is modulated by respiratory activity which indicates the existence of direct interactions between the respiratory and sympathetic networks within the brainstem. Our experimental studies reveal that T(E) prolongation evoked by baroreceptor stimulation varies with respiratory phase and depends on the pons. We speculate that the sympathetic baroreceptor reflex, providing negative feedback from baroreceptors to the rostral ventrolateral medulla and SNA, has two pathways: one direct and independent of the respiratory-sympathetic interactions and the other operating via the respiratory pattern generator and is hence dependent on the respiratory modulation of SNA. Our experimental studies in the perfused in situ rat preparation and complementary computational modelling studies support the hypothesis that baroreceptor activation during expiration prolongs the T(E) via transient activation of post-inspiratory and inhibition of augmenting expiratory neurones of the Bötzinger Complex (BötC). We propose that these BötC neurones are also involved in the respiratory modulation of SNA, and contribute to the respiratory modulation of the sympathetic baroreceptor reflex.
交感神经活动(SNA)受呼吸活动调节,这表明脑干内呼吸和交感网络之间存在直接相互作用。我们的实验研究表明,由压力感受器刺激引起的 T(E)延长随呼吸相而变化,并取决于脑桥。我们推测,交感压力感受器反射,即从压力感受器向延髓腹外侧头端和 SNA 提供负反馈,有两条途径:一条是直接的,不依赖于呼吸-交感相互作用,另一条是通过呼吸模式发生器起作用,因此依赖于 SNA 的呼吸调节。我们在灌流原位大鼠制备中的实验研究和补充的计算模型研究支持这样的假设,即在呼气期间激活压力感受器可通过短暂激活吸气后神经元和抑制吸气后神经元来延长 T(E)增强呼气神经元的 Bötzinger 复合体(BötC)。我们提出,这些 BötC 神经元也参与了 SNA 的呼吸调节,并有助于交感压力感受器反射的呼吸调节。