Dilating forces on the upper airway of anesthetized dogs.
We reasoned that in an isolated sealed upper airway a pressure change would be caused by a change in airway volume. In eight spontaneously breathing anesthetized dogs, we isolated the upper airway by transecting the cervical trachea and sealing it from the lung and from the atmosphere. Pressure changes in this isolated upper airway were studied in relation to respiratory phase as evidenced by alae nasi electromyographic (EMG) activation and tidal volume measured at the distal trachea. A fall in pressure, indicating airway dilation, occurred with each spontaneous respiratory effort. Like the moving average of the alae nasi EMG, the pressure drop reached a peak value early in inspiration, was inhibited by further lung inflation, and was absent during passive mechanical ventilation. End-expiratory tracheal occlusion or vagotomy prolonged and augmented EMG activity and also the inspiratory fall in upper airway pressure. Increased levels of CO2 increased the magnitude of change in pressure during inspiration. An inhibiting effect of lung inflation was present to an equal extent at low and high levels of chemical drive. We show that dilation of the airway is concurrent with upper airway muscle activation during early inspiration, that this dilation increases with increasing chemical drive, and that vagal reflexes during lung inflation inhibit this dilation during the latter half of inspiration.
D000403:Airway Resistance; D000818:Animals; D004285:Dogs; D004576:Electromyography; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000502:physiology*; D011312:Pressure; D012018:Reflex / Q000502:physiology; D012119:Respiration; D012121:Respiration, Artificial; D013990:Tidal Volume; D014132:Trachea / Q000502:physiology*; D014630:Vagus Nerve / Q000502:physiology; D014939:Work of Breathing