Chesrown S E, Venugopalan C S, Gold W M, Drazen J M
J Clin Invest. 1980 Feb;65(2):314-20. doi: 10.1172/JCI109674.
To determine if electrical stimulation of autonomic nerves could excite nonadrenergic inhibitory motor pathways in the guinea pig respiratory system in vivo, we studied the effects of electrical stimulation of the cervical vagi and sympathetic nerve trunks on pressure changes (P(p)) within an isolated, fluid-filled cervical tracheal segment which reflected changes in trachealis muscle tone. We preserved the innervation and circulation of the segment as evidenced by a rise in P(p) with vagus nerve stimulation and a fall in P(p) with intravenous isoproterenol. In five atropine-treated animals, stimulation of the cut vagi or sympathetic nerve trunks resulted in a mean fall in P(p) of 7.9 and 8.2 cm H(2)O, respectively. Treatment with propranolol attenuated the response to sympathetic stimulation but not vagal stimulation. To determine if these relaxation responses were mediated by an adrenergic or nonadrenergic mechanism, we studied an additional five animals that had been treated with 6-hydroxydopamine to destroy adrenergic nerve endings. In 6-hydroxydopamine, atropine, and propranolol-treated animals, sympathetic nerve stimulation decreased P(p) only 0.65 cm H(2)O, confirming the elimination of adrenergic nerve influences, whereas vagus nerve stimulation decreased P(p) 17.7 cm H(2)O. After sectioning the recurrent laryngeal nerves, the mean decrease in P(p) during vagus nerve stimulation was only 3.2 cm H(2)O. These findings demonstrate the presence of nonadrenergic inhibitory nerves in the guinea pig trachea in vivo. They further show that nonadrenergic inhibitory nerve effects are elicited during electrical stimulation of the vagus nerves and that interruption of the recurrent laryngeal nerves diminishes the magnitude of these effects.
为了确定自主神经的电刺激是否能在体内激发豚鼠呼吸系统中的非肾上腺素能抑制性运动通路,我们研究了颈迷走神经和交感神经干的电刺激对分离的、充满液体的颈段气管内压力变化(P(p))的影响,该压力变化反映了气管肌紧张度的变化。我们保留了该节段的神经支配和血液循环,迷走神经刺激时P(p)升高以及静脉注射异丙肾上腺素时P(p)降低证明了这一点。在5只经阿托品处理的动物中,刺激切断的迷走神经或交感神经干分别导致P(p)平均下降7.9和8.2 cm H₂O。普萘洛尔治疗减弱了对交感神经刺激的反应,但对迷走神经刺激无影响。为了确定这些舒张反应是由肾上腺素能还是非肾上腺素能机制介导的,我们研究了另外5只经6-羟基多巴胺处理以破坏肾上腺素能神经末梢的动物。在经6-羟基多巴胺、阿托品和普萘洛尔处理的动物中,交感神经刺激仅使P(p)降低0.65 cm H₂O,证实了肾上腺素能神经影响已消除,而迷走神经刺激使P(p)降低17.7 cm H₂O。切断喉返神经后,迷走神经刺激期间P(p)的平均降低仅为3.2 cm H₂O。这些发现证明了豚鼠气管在体内存在非肾上腺素能抑制神经。它们进一步表明,在迷走神经电刺激期间会引发非肾上腺素能抑制神经效应,并且喉返神经的中断会减小这些效应的幅度。