Cough reflex is additively potentiated by inputs from the laryngeal and tracheobronchial [corrected] receptors and enhanced by stimulation of the central respiratory neurons.

Abstract

The cough is an essential airway defense reflex. In this study we investigated the coordination of inputs from the laryngeal and tracheobronchial receptors in the cough reflex. In 15 beagle dogs (7-9 kg) lightly anesthetized with intravenous profobol (20-30 mg/kg/h), the cough response was elicited with mechanical stimulation of either the vocal chord or tracheal bifurcation. Simultaneous stimulation of both sites increased all the parameters of cough strength, that is, mean pleural pressure (P (pl)), mean expiratory flow, number of cough bouts, and cough duration, in comparison with stimulation of the sites individually. The increases in mean P (pl) and cough duration reached statistical significance (13.3 vs. 18.4 cmH(2)O and 13.3 vs. 18.2 s, respectively). When the anesthetic level became deeper, the prolongation of cough duration almost disappeared, but the augmentation of mean P (pl) was much less affected. During stimulation of the central respiratory neurons by intravenous dimorphoramine or acute hyperoxic hypercapnia, the cough strength increased significantly. We concluded that inputs from the laryngeal and tracheobonchial cough receptors acted in concert and potentiated the cough reflex. Furthermore, stimulation of the central respiratory neurons may increase the intensity of a cough response.