Roberts A M, Kaufman M P, Baker D G, Brown J K, Coleridge H M, Coleridge J C
J Appl Physiol Respir Environ Exerc Physiol. 1981 Aug;51(2):485-93. doi: 10.1152/jappl.1981.51.2.485.
Bradykinin stimulates the afferent vagal endings of bronchial C-fibers but has little effect on other pulmonary vagal afferents. In anesthetized dogs with open chest, we recorded transverse tension in the posterior wall (trachealis muscle) of an upper cervical tracheal segment and stimulated bronchial C-fibers selectively by injecting bradykinin (19 ng-3 microgram) into a bronchial artery. The recurrent and pararecurrent laryngeal nerves were cut so that the superior laryngeal nerves provided the motor supply to the segment. Bradykinin caused a dose-dependent increase in tracheal muscle tension and often a conspicuous decrease in heart rate, which were abolished by vagotomy or administration of atropine. Injection of bradykinin still evoked tracheal contraction when myelinated lung afferents were blocked by cooling the midcervical vagi to 7 degrees C, but contraction was abolished when unmyelinated lung afferents were blocked by cooling to 0-1 degrees C, the effects of cooling being reversible. Our results indicate that stimulation of bronchial C-fibers, like that of pulmonary C-fibers, evokes reflux contraction of airway smooth muscle and reflex cardiac slowing.
缓激肽刺激支气管C纤维的传入迷走神经末梢,但对其他肺迷走神经传入几乎没有影响。在开胸麻醉犬中,我们记录了颈上段气管后壁(气管肌)的横向张力,并通过向支气管动脉注射缓激肽(19纳克 - 3微克)选择性刺激支气管C纤维。切断喉返神经和喉返旁神经,使喉上神经为该节段提供运动神经支配。缓激肽导致气管肌紧张度呈剂量依赖性增加,且常伴有心率显著下降,迷走神经切断术或给予阿托品可消除这些反应。当通过将颈中部迷走神经冷却至7摄氏度阻断有髓肺传入神经时,注射缓激肽仍能诱发气管收缩,但当通过冷却至0 - 1摄氏度阻断无髓肺传入神经时,收缩反应消失,冷却的影响是可逆的。我们的结果表明,刺激支气管C纤维,与刺激肺C纤维一样,会引起气道平滑肌的反射性收缩和反射性心率减慢。