Blockade of pulmonary stretch receptors reinforces diaphragmatic activity during high-frequency oscillatory ventilation.

During apneic periods elicited by high-frequency oscillatory ventilation (HFOV) a tonic diaphragmatic activity was observed, contrasting with the absence of diaphragmatic activity during apnea induced by lung inflation. To clarify the mechanism underlying the persistence of the diaphragmatic activity during HFOV-induced arrest of breathing the reflex responses to short periods of HFOV, and to periods of lung inflation with airway pressure (Paw) equal to the mean Paw and/or to maximal Paw during HFOV were examined both before and after the blockade of slowly adapting stretch receptors (SR) by inhalation of sulphur dioxide (SO2) in anaesthetized rabbits. In animals with intact SR, the HFOV-induced reflex apnea lasted longer than that induced by lung inflation, the associated diaphragmatic activity being in the most cases higher than the diaphragmatic activity during quiet expiration; inflation, however, completely inhibited diaphragmatic activity. After blockade of SR, spontaneous breathing continued during periods of lung inflation, i.e., the Hering-Breuer inflation reflex was abolished, whereas HFOV still led to a cessation of spontaneous breathing, the associated diaphragmatic activity even exceeding the level observed during quiet inspiration. From these results we conclude that only one part of the reflex response to HFOV is due to SR-stimulation and that in addition other vagal pulmonary receptors (irritant- and/or C-fibre-receptors) are involved. The stimulation of the latter counterbalances the concomitant stimulation of SR, giving rise to the tonic activity of the diaphragm.