We utilised a tracheostomised, unanaesthetised, sleeping dog model to study the reflex effects on inspiratory motor output of low-amplitude, highfrequency pressure oscillations (HFPO) applied to the isolated upper airway (UA). HFPO (30 Hz and ±2 to ±4 cmH20) were applied via a piston pump during eupnoea, inspiratory resistive-loading and trachéal occlusions. When applied to the patent UA during expiration, and especially during late expiration, HFPO prolonged expiratory time and tonically activated the genioglossus muscle EMG. When applied to the patent UA during inspiration, HFPO caused inhibition of inspiratory motor output by either: a) a shortening of T1, as inspiration was terminated coincident with the onset of HFPO; or b) a prolonged T, accompanied by a decreased rate of rise of diaphragm EMG (EMGD1/T1,) and rate of fall of trachéal pressure (PTn/T,). These effects of HFPO were observed during eupnoea and inspiratory resistive-loading, but were maximal during trachéal occlusions where the additional inhibitory effects of lung inflation reflexes were minimised. During eupnoea, topical anaesthesia of the UA abolished the HFPO-induced prolongation of TE, suggesting that the response was mediated primarily by mechanoreceptors close to the mucosal surface; whereas the TE prolonging effects of a square-wave of negative pressure (range -4.0 to -14.9 cmH20) sufficient to close the airway were preserved following anaesthesia. These results demonstrate that high-frequency, low-amplitude oscillatory pressure waves in the UA, similar to those found in snoring, produce reflex inhibition of inspiratory motor output. This reflex may help maintain UA patency by decreasing the collapsing pressure generated by the inspiratory pump muscles and transmitted to the UA.
Bibliographical noteInhibition of inspiratory motor output
- Diaphragm EMG
- Reflexes nomination for prizes: Nil