A novel procedure for mediastinal vagotomy inhibits neurogenic inflammation in rat bronchial tree

Abstract

Tachykinin-containing sensory axons originating from the cervical vagal nerves and the first several pairs of thoracic spinal nerves are involved in neurogenic inflammation evoked by capsaicin in the bronchial tree. Unilateral degeneration of the cervical vagal trunk by surgical lesion inhibits neurogenic inflammation in the ipsilateral bronchial airways. The vagal trunk has two main branches, the thoracic vagus nerve and recurrent laryngeal nerve in the thorax. The main purpose of this study was to determine whether the thoracic vagus nerve or recurrent laryngeal nerve was significantly involved in the neural control of bronchial inflammation in the rat. A novel and safe surgical procedure was used for selectively cutting the right thoracic vagal trunk, thoracic vagus nerve, or recurrent laryngeal nerve by introducing the surgical instrument through an aperture between the first and second ribs in the ventral wall of the rostral mediastinum. This surgical operation could be completed without causing a pneumothorax. After 2 postoperative weeks, the effects of denervation on capsaicin-induced plasma extravasation in the respiratory tract were tested. Either right thoracic vagal trunk transection or thoracic vagus section significantly decreased plasma extravasation in the right bronchial tree. Thoracic vagus section was obviously more effective. Evans blue extravasation in the right lobar bronchi was reduced by 44–78% after thoracic vagal trunk transection, while that in the right mainstem and lobar bronchi was reduced by 58–81% after thoracic vagus section. Area densities of India ink-labeled leaky blood vessels in the right lobar bronchi were reduced by 40–65% after thoracic vagal trunk transection, and those in the right mainstem and lobar bronchi were reduced by 83–88% after thoracic vagus neurectomy. Recurrent laryngeal neurectomy did not change the plasma extravasation induced by capsaicin in the trachea and bronchi. These results suggest that capsaicin-sensitive fibers running in the vagal trunk, which largely mediated neurogenic inflammation in the bronchial tree, were projected into the thoracic vagus nerve which, in turn, sent these nerve fibers to the ipsilateral bronchial tree. For the trachea, the remaining sensory fibers surviving denervation might provide sufficient tachykinins to trigger neurogenic inflammation.