An efferent pathway mediating reflex tracheal dilation in awake dogs

1984 ◽  
Vol 57 (2) ◽  
pp. 413-418 ◽  
Author(s):  
G. Bowes ◽  
E. J. Shakin ◽  
E. A. Phillipson ◽  
N. Zamel

Lung inflation is known to produce reflex relaxation of tracheal smooth muscle (TSM) and dilation of the upper airway, but the specific efferent pathway involved has not been established. Therefore we examined TSM tone in four trained awake dogs by measuring pressure changes in the water-filled cuff of an endotracheal tube that was inserted into the lower cervical trachea through a permanent tracheostomy. Under control conditions, sustained lung inflation with 1 liter of air produced apnea (Hering-Breuer inflation reflex) and a decrease in cuff pressure (Pcuff) of 37.4 +/- 12.0 (mean +/- SD) cmH2O. beta-Adrenergic blockade with propranolol had no effect on either the apneic or TSM responses to lung inflation. Efferent parasympathetic blockade with atropine sulfate (1.2–2.4 mg) abolished TSM tone, which was then restored to control levels by a continuous intravenous infusion of serotonin (14–28 micrograms X kg-1 X min-1). Under these conditions, lung inflation still induced reflex apnea but no longer relaxed TSM tone (mean decrease in Pcuff, 2.7 +/- 1.4 cmH2O, P less than 0.001). The findings indicate that reflex tracheal dilation in response to lung inflation is mediated by an efferent cholinergic (parasympathetic) pathway.

1985 ◽  
Vol 58 (2) ◽  
pp. 452-458 ◽  
Author(s):  
K. P. Strohl ◽  
J. M. Fouke

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.


1986 ◽  
Vol 61 (3) ◽  
pp. 912-918 ◽  
Author(s):  
J. M. Fouke ◽  
J. P. Teeter ◽  
K. P. Strohl

The study was performed to investigate the relationship between force generation and upper airway expansion during respiratory efforts by upper airway muscles. In 11 anesthetized dogs we isolated the upper airway (nasal, oral, pharyngeal, and laryngeal regions) by transecting the cervical trachea and sealing the nasal and oral openings. During spontaneous respiratory efforts the pressure within the sealed upper airway, used as an index of dilating force, decreased during inspiration. On alternate breaths the upper airway was opened to a pneumotachograph, and an increase in volume occurred, also during inspiration. Progressive hyperoxic hypercapnia produced by rebreathing increased the magnitude of change in pressure and volume. At any level of drive, peak pressure or volume occurred at the same point during inspiration. At any level of drive, volume and pressure changes increased with end-expiratory occlusion of the trachea. The force-volume relationship determined from measurements during rebreathing was compared with pressure-volume curves performed by passive inflation of the airway while the animal was apneic. The relationship during apnea was 1.06 +/- 0.55 (SD) ml/cmH2O, while the force-volume relationship from rebreathing trials was -1.09 +/- 0.45 ml/cmH2O. We conclude that there is a correspondence between force production and volume expansion in the upper airway during active respiratory efforts.


1992 ◽  
Vol 72 (6) ◽  
pp. 2311-2316 ◽  
Author(s):  
H. Miki ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
M. Satoh ◽  
...  

We examined the effect of electrical stimulation of the hypoglossal nerve and pharyngeal lubrication with artificial surfactant (Surfactant T-A) on the opening of obstructed upper airway in nine anesthetized supine dogs. The upper airway was isolated from the lower airway by transecting the cervical trachea. Upper airway obstruction was induced by applying constant negative pressures (5, 10, 20, and 30 cmH2O) on the rostral cut end of the trachea. Peripheral cut ends of the hypoglossal nerves were electrically stimulated by square-wave pulses at various frequencies from 10 to 30 Hz (0.2-ms duration, 5–7 V), and the critical stimulating frequency necessary for opening the obstructed upper airway was measured at each driving pressure before and after pharyngeal lubrication with artificial surfactant. The critical stimulation frequency for upper airway opening significantly increased as upper airway pressure became more negative and significantly decreased with lubrication of the upper airway. These findings suggest that greater muscle tone of the genioglossus is needed to open the occluded upper airway with larger negative intraluminal pressure and that lubrication of the pharyngeal mucosa with artificial surfactant facilitates reopening of the upper airway.


2000 ◽  
Vol 89 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Robert L. Coon ◽  
Patrick J. Mueller ◽  
Philip S. Clifford

The canine cervical trachea has been used for numerous studies regarding the neural control of tracheal smooth muscle. The purpose of the present study was to determine whether there is lateral dominance by either the left or right vagal innervation of the canine cervical trachea. In anesthetized dogs, pressure in the cuff of the endotracheal tube was used as an index of smooth muscle tone in the trachea. After establishment of tracheal tone, as indicated by increased cuff pressure, either the right or left vagus nerve was sectioned followed by section of the contralateral vagus. Sectioning the right vagus first resulted in total loss of tone in the cervical trachea, whereas sectioning the left vagus first produced either a partial or no decrease in tracheal tone. After bilateral section of the vagi, cuff pressure was recorded during electrical stimulation of the rostral end of the right or left vagus. At the maximum current strength used, stimulation of the left vagus produced tracheal constriction that averaged 28.5% of the response to stimulation of the right vagus (9.0 ± 1.8 and 31.6 ± 2.5 mmHg, respectively). In conclusion, the musculature of cervical trachea in the dog appears to be predominantly controlled by vagal efferents in the right vagus nerve.


2021 ◽  
Vol 65 (6) ◽  
pp. 439
Author(s):  
GP Deepak ◽  
Rakesh Kumar ◽  
Munisha Agarwal ◽  
Manoj Bharadwaj ◽  
NeeraG Kumar ◽  
...  

1984 ◽  
Vol 18 ◽  
pp. 397A-397A
Author(s):  
Oommen P Mathew ◽  
John T Fisher ◽  
Franca B Sant'Ambrogio ◽  
Giuseppe Sant'Ambrogio

1986 ◽  
Vol 61 (3) ◽  
pp. 1091-1097 ◽  
Author(s):  
E. C. Deal ◽  
M. A. Haxhiu ◽  
M. P. Norcia ◽  
J. Mitra ◽  
N. S. Cherniack

These studies investigated the role of the intermediate area of the ventral surface of the medulla (VMS) in the tracheal constriction produced by hypercapnia. Experiments were performed in chloralose-anesthetized, paralyzed, and artificially ventilated cats. Airway responses were assessed from pressure changes in a bypassed segment of the rostral cervical trachea. Hyperoxic hypercapnia increased tracheal pressure and phrenic nerve activity. Intravenous atropine pretreatment or vagotomy abolished the changes in tracheal pressure without affecting phrenic nerve discharge. Rapid cooling of the intermediate area reversed the tracheal constriction produced by hypercapnia. Graded cooling produced a progressive reduction in the changes in maximal tracheal pressure and phrenic nerve discharge responses caused by hypercapnia. Cooling the intermediate area to 20 degrees C significantly elevated the CO2 thresholds of both responses. These findings demonstrate that structures near the intermediate area of the VMS play a role in the neural cholinergic responses of the tracheal segment to CO2. It is possible that neurons or fibers in intermediate area influence the motor nuclei innervating the trachea. Alternatively, airway tone may be linked to respiratory motor activity so that medullary interventions that influence respiratory motor activity also alter bronchomotor tone.


1979 ◽  
Vol 7 (2) ◽  
pp. 152-157 ◽  
Author(s):  
W. R. Thompson ◽  
T. E. Oh

Increases in endotracheal tube cuff volume and pressure during anaesthesia have been reported to be due to the diffusion of nitrous oxide into the cuff. This study compared cuff volume and pressure changes in anaesthetized intubated patients who were ventilated with those allowed to breath spontaneously. The cuffs of Magill red rubber endotracheal tubes were inflated with either air or a nitrous oxide-oxygen mixture. Serial pressure and volume recordings confirmed that both parameters increased when the cuff was inflated with air. The increase in cuff pressure was however, greater during intermittent positive pressure ventilation than for spontaneous respiration. There were no significant changes when the cuff was inflated with the nitrous oxide-oxygen mixture.


1998 ◽  
Vol 84 (3) ◽  
pp. 1063-1075 ◽  
Author(s):  
P. R. Eastwood ◽  
A. K. Curran ◽  
C. A. Smith ◽  
J. A. Dempsey

To determine the effect of upper airway (UA) negative pressure and collapse during inspiration on regulation of breathing, we studied four unanesthetized female dogs during wakefulness and sleep while they breathed via a fenestrated tracheostomy tube, which was sealed around the permanent tracheal stoma. The snout was sealed with an airtight mask, thereby isolating the UA when the fenestration (Fen) was closed and exposing the UA to intrathoracic pressure changes, but not to flow changes, when Fen was open. During tracheal occlusion with Fen closed, inspiratory time (Ti) increased during wakefulness, non-rapid-eye-movement (NREM) sleep and rapid-eye-movement (REM) sleep (155 ± 8, 164 ± 11, and 161 ± 32%, respectively), reflecting the removal of inhibitory lung inflation reflexes. During tracheal occlusion with Fen open (vs. Fen closed): 1) the UA remained patent; 2) Ti further increased during wakefulness and NREM (215 ± 52 and 197 ± 28%, respectively) but nonsignificantly during REM sleep (196 ± 42%); 3) mean rate of rise of diaphragm EMG (EMGdi/Ti) and rate of fall of tracheal pressure (Ptr/Ti) were decreased, reflecting an additional inhibitory input from UA receptors; and 4) both EMGdi/Ti and Ptr/Ti were decreased proportionately more as inspiration proceeded, suggesting greater reflex inhibition later in the effort. Similar inhibitory effects of exposing the UA to negative pressure (via an open tracheal Fen) were seen when an inspiratory resistive load was applied over several breaths during wakefulness and sleep. These inhibitory effects persisted even in the face of rising chemical stimuli. This inhibition of inspiratory motor output is alinear within an inspiration and reflects the activation of UA pressure-sensitive receptors by UA distortion, with greater distortion possibly occurring later in the effort.


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