Neurophysiological effects of recurrent laryngeal and thoracic vagus nerves on mediating the neurogenic inflammation of the trachea, bronchi, and esophagus of rats.

The present study aims to investigate the neurophysiological effects of recurrent laryngeal nerve and thoracic vagus nerve on the non-cholinergic regulation of neurogenic plasma extravasation of the rat trachea, bronchi, and esophagus. Through thoracotomy, three nerve components, the right thoracic vagal trunk, thoracic vagus nerve, and recurrent laryngeal nerve, were identified. The experiment was sequentially conducted in four steps. First, the individual nerve component was electrically stimulated and the induced inflammatory responses, as quantified by the area density of India ink-labelled blood vessels in the trachea, bronchial trees and esophagus, were compared. Second, we assessed the relative importance of medial and lateral side of the right thoracic vagus nerve in inducing the inflammatory responses by alternative stimulation of one side with simultaneous severance of the other side of this nerve. Third, we examined the effects of transection of the lateral half of the right thoracic vagus nerve on the degeneration of axon fibers located at the following three sites: the nerve segment proximal to cutting site, bronchial and esophageal nerve branches. Finally, we directly observed the inflammatory histopathology of the right lower trachea after stimulation of the medial half of the right thoracic vagus nerve with transection of its lateral half. In this study, we found that the right recurrent laryngeal nerve was predominant in mediating the neurogenic inflammatory responses of upper and dorsal portions of trachea, whereas the right thoracic vagus nerve was predominant in mediating those of the right lower ventral wall of trachea, right main bronchus, and right lobar bronchial trees. The axon fibers of the right thoracic vagus nerve responsible for mediating the neurogenic inflammatory responses of the right lower ventral trachea were mainly accumulated in the medial half, whereas those innervating the right main bronchus, right lobar bronchial trees, and lower esophagus were largely in the lateral half of this nerve. Transection of the lateral half of the right thoracic vagus nerve resulted in significant degeneration of myelinated fibers in its bronchial and esophageal nerve branches. Histopathological examination of the right lower trachea after electrical stimulation of the medial half of thoracic vagus nerve demonstrated the silver-stained leaky venules with accumulations of inflammatory cells. We thus concluded that afferent C-fibers to upper and dorsal portions of trachea were mainly from recurrent laryngeal nerve. In contrast, the neurogenic inflammatory responses of the right lower trachea were predominantly mediated by the medial half of the right thoracic vagus nerve, and those of the right main bronchus, bronchial trees and lower esophagus were largely by the lateral half of this nerve.