Characteristics of sustained graded inspiratory inhibition by phasic lung volume changes

1980 ◽  
Vol 48 (2) ◽  
pp. 302-307 ◽  
Author(s):  
J. P. Baker ◽  
J. E. Remmers

The dynamic characteristics of graded reversible inspiratory inhibition by vagal feedback were investigated in pentobarbital-anesthetized paralyzed cats, ventilated with a servo respirator. The volume and time associated with various levels of graded inhibition were determined by using a series of constant-flow lung inflations. Protracted phrenic inhibition was produced by lung inflation, which was arrested when the phrenic discharge was partially inhibited. Thereafter, the volume was withdrawn along a trajectory that approximately paralleled the fall in inhibitory threshold. This volume-withdrawal trajectory would be expected to produce a sustained nearly constant level of inhibition based on the results determined from the constant-flow inflations. However, the observed inhibition exceeded that expected, increasing to a maximum and then decreasing to expected values over a period ranging from 1 to 2 s in most animals. This excess inhibition cannot be attributed to the known dynamic properties of pulmonary stretch receptors; their activity should be reduced, for any particular lung volume, during the volume withdrawal maneuver. These results suggest a central integrative processing of vagal afferent activity that causes inhibition to lag volume. This delay acts to promote inspiratory off-switching because it prevents the development of a protracted period of reversible inhibition.

1975 ◽  
Vol 38 (5) ◽  
pp. 869-874 ◽  
Author(s):  
M. M. Grunstein ◽  
I. Wyszogrodski ◽  
J. Milic-Emili

In six spontaneously breathing anesthetized cats, intermittently subjected to inspiratory elastic loads, we have studied the relationships between tidal volume (VT) and the durations of inspiration (Ti) and breath duration (Ttot) obtained during spontaneous ventilation from resting lung volume (FRCc) and from elevated end-expiratory levels. The latter was elevated by submerging the expiratory breathing line into a column of water, representing the addition of an expiratory threshold load (ETL). The VT vs. Ti relationships obtained at different end-expiratory levels were similar, indicating that during ETL the vagal mechanism regulating Ti responds only to lung volume changes above the new end-expiratory level and is independent of the absolute end-expiratory lung volume. Single vagal fiber recordings suggest that this effect on Ti control may be explained on the basis of adaptation occurring at the level of the pulmonary stretch receptors. The control of Ttot, on the other hand, was found to depend both on the Ti of the preceding breath (phasic component) and on a separate vagal mechanism specifically affecting the duration of expiration (Te) in response to changes in the absolute end-expiratory lung volume. The latter mechanism is functionally inoperative at FRCc.


1992 ◽  
Vol 73 (2) ◽  
pp. 701-707 ◽  
Author(s):  
W. M. St John ◽  
D. Zhou

We evaluated the hypothesis that the tonic discharge of pulmonary stretch receptors significantly influences the respiratory-modulated activities of cranial nerves. Decerebrate and paralyzed cats were ventilated with a servo-respirator, which produced changes in lung volume in parallel with integrated phrenic activity. Activities of the facial, hypoglossal, and recurrent laryngeal nerves and nerves to the thyroarytenoid muscle and triangularis sterni were recorded. After a stereotyped pattern of lung inflation, tracheal pressure was held at 1, 2, 4, or 6 cmH2O during the subsequent ventilatory cycle. Increases in tracheal pressure caused progressive reductions in both inspiratory and expiratory cranial nerve activities and progressive elevations in triangularis sterni discharge; peak levels of phrenic activity declined modestly. Similar changes were observed in normocapnia and hypercapnia. We conclude that the tonic discharge of pulmonary stretch receptors is an important determinant of the presence and magnitude of respiratory-modulated cranial nerve activity. This reflex mechanism may maintain upper airway patency and also regulate expiratory airflow.


1981 ◽  
Vol 59 (9) ◽  
pp. 1017-1021 ◽  
Author(s):  
C. Gaultier ◽  
J. P. Mortola

The apnea following lung inflation (Hering–Breuer expiratory promoting reflex) is a vagally mediated reflex which is initiated by the activation of pulmonary stretch receptors (PSR) and terminated by the interaction of several factors, which include adaptation of PSR, chemical stimuli, level of anaesthesia, and body temperature. Since PSR activity is determined by the changes in airway tension, the interpretation of the strength of vagal reflexes on the basis of changes in lung volume rather than transpulmonary pressure can be misleading when the mechanical properties of the respiratory system are not constant. In this study we compared the reflex apnea resulting from lung inflation of young and adult mammals, the respiratory system of which have very different mechanical properties. If the response is compared on the basis of similar changes in lung volume, it can be considered weaker or stronger in the young depending upon the normalizing parameter used. However, when considered on the basis of the relative changes in transpulmonary pressure, which better reflects the activation of PSR, the reflex is weaker in young rats and rabbits than in their adult counterparts and similar in dogs. The analysis of the underlying mechanisms suggests a weaker vagal contribution in the young animal, but a satisfactory conclusion requires a better knowledge of the factors which, in the younger animals, result in the termination of the apnea.


1986 ◽  
Vol 61 (1) ◽  
pp. 192-197 ◽  
Author(s):  
G. M. Barnas ◽  
R. B. Banzett ◽  
M. B. Reid ◽  
J. Lehr

We recorded the responses of 21 slowly adapting pulmonary stretch receptors (PSRs) and 8 rapidly adapting pulmonary stretch receptors (RARs) from the vagi of anesthetized open-chest dogs to high-frequency ventilation (HFV) at 15 Hz, at constant mean end-expiratory lung volume, and constant end-tidal PCO2. HFV applied in this way has been shown to prolong expiration. The responses of pulmonary afferents during HFV at constant mean volume have not been described. In the present experiments, receptor discharge during HFV was compared with that during the end-expiratory pause of normal-frequency ventilation. Average PSR discharge increased when HFV was applied, although not all PSRs exhibited increases. RARs were generally silent during normal and high-frequency ventilation at functional residual capacity and above. However, at low lung volumes, RAR discharge increased greatly when HFV was applied. We conclude that PSR discharge is increased during HFV in the absence of increased lung volume and that increases in PSR discharge during HFV are sufficient to explain the reflex that prolongs expiration in dogs.


1987 ◽  
Vol 58 (6) ◽  
pp. 1259-1274 ◽  
Author(s):  
A. J. Berger ◽  
T. E. Dick

1. Intracellular recordings were made from 50 dorsal respiratory group (DRG) neurons in the region of the ventrolateral nucleus of the solitary tract in anesthetized, paralyzed cats ventilated with a cycle-triggered pump whose inflation stroke was triggered by the onset of phrenic nerve inspiratory (I) discharge. Activity was recorded simultaneously in the ipsilateral nodose ganglion from sensory cell bodies of slowly adapting pulmonary stretch receptors (PSRs). 2. Respiratory cycle-related membrane potential changes of DRG neurons were recorded. Twenty-six neurons that did not exhibit spikes were classified as I alpha, I beta or pump (P)-cells by comparing their membrane potential trajectories during I in the presence of lung inflation with that observed during I, but with lung inflation withheld. The remaining 24 neurons were classified similarly, but the classification was based upon a comparison of their I-phase spike activity responses with and without lung inflation. I phase-related histograms of either membrane potential or spike activity were constructed to facilitate DRG neuronal classification. Additionally, steady lung inflation of varying magnitudes was applied during the expiratory phase. This prolonged expiration and produced different responses in the neurons. Generally, I beta and P-cells were depolarized, whereas I alpha cells were hyperpolarized. 3. Low-intensity electrical stimulation of the ipsilateral vagus nerve evoked excitatory postsynaptic potentials (EPSPs) in all three DRG neuronal types. P-cells and I beta cells exhibited EPSPs in response to the lowest intensity; generally this intensity was below threshold for the simultaneously recorded PSR. Overall, EPSPs in I alpha cells had the highest thresholds, but some EPSPs could be evoked at thresholds similar to those of the I beta cells. The distributions of the average onset latency of the evoked EPSP overlapped considerably. Thus vagal electrical stimulation cannot be used for unequivocal classification of DRG neurons into I alpha, I beta, and P-cell subpopulations. 4. Using intracellular spike-triggered averaging, single PSRs were shown to generate monosynaptic EPSPs in I beta neurons and P-cells but not I alpha cells. Divergence of single PSR afferents also was observed. Relationships between EPSP shape factors, amplitudes, and PSR afferent conduction velocity are similar to those previously observed for monosynaptic EPSPs in hindlimb motoneurons generated by spinal afferents.


2000 ◽  
Vol 279 (5) ◽  
pp. R1606-R1618 ◽  
Author(s):  
Mislav Tonkovic-Capin ◽  
Edward J. Zuperku ◽  
Eckehard A. Stuth ◽  
Jurica Bajic ◽  
Zoran Dogas ◽  
...  

The purpose of these studies is to better understand the nature of the reflex interactions that control the discharge patterns of caudal medullary, expiratory (E) bulbospinal neurons. We examined the effect of central chemodrive inputs measured as arterial CO2 tension (PaCO2 ) during hyperoxia on the excitatory and inhibitory components of the lung inflation responses of these neurons in thiopental sodium-anesthetized, paralyzed dogs. Data from slow ramp inflation and deflation test patterns, which were separated by several control inflation cycles, were used to produce plots of neuronal discharge frequency ( F n) versus transpulmonary pressure (Pt). Pt was used as an index of the activity arising from the slowly adapting pulmonary stretch receptors (PSRs). Changes in inspired CO2 concentrations were used to produce PaCO2 levels that ranged from 20 to 80 mmHg. The data obtained from 41 E neurons were used to derive an empirical model that quantifies the average relationship for F n versus both Pt and PaCO2 . This model can be used to predict the time course and magnitude of E neuronal responses to these inputs. These data suggest that the interaction between PaCO2 and PSR-mediated excitation and inhibition of F n is mainly additive, but synergism between PaCO2 and excitatory inputs is also present. The implications of these findings are discussed.


1987 ◽  
Vol 62 (5) ◽  
pp. 1912-1916 ◽  
Author(s):  
P. S. Clifford ◽  
L. B. Bell ◽  
F. A. Hopp ◽  
R. L. Coon

The Breuer-Hering reflex (BHR) reappears 12–14 wk after surgical lung denervation in beagle dogs (J. Appl. Physiol. 54: 1451–1456, 1983). To demonstrate that this is due to reinnervation of pulmonary stretch receptors, we recorded nerve activity from regenerated branches of the left vagus nerve in five beagle dogs. Ten days postdenervation the BHR was absent, whereas by 19 mo it was clearly present. Multifiber pulmonary afferent activity was observed in all five dogs with single-fiber activity observed in three. Sectioning the right vagus nerve did not alter the BHR, but sectioning all the regenerated branches of the left vagus abolished the reflex. In two additional dogs studied 17 mo postsurgery, recordings were made from few fiber nerve bundles of the left cervical vagus. Nerve activity was increased during gentle stroking of the surface of the left upper and lower lobes, indicating receptive fields in both lobes. These data demonstrate that reinnervation of pulmonary stretch receptors does occur and provides evidence that reinnervation of these receptors is responsible for return of the BHR after pulmonary denervation.


2006 ◽  
Vol 101 (2) ◽  
pp. 609-617 ◽  
Author(s):  
E. Fiona Bailey ◽  
Ralph F. Fregosi

Here we review the influence of bronchopulmonary receptors (slowly and rapidly adapting pulmonary stretch receptors, and pulmonary/bronchial C-fiber receptors) on respiratory-related motor output to upper airway muscles acting on the larynx, tongue, and hyoid arch. Review of the literature shows that all muscles in all three regions are profoundly inhibited by lung inflation, which excites slowly adapting pulmonary stretch receptors. This widespread coactivation includes the recruitment of muscles that have opposing mechanical actions, suggesting that the stiffness of upper airway muscles is highly regulated. A profound lack of information on the modulation of upper airway muscles by rapidly adapting receptors and bronchopulmonary C-fiber receptors prohibits formulation of a conclusive opinion as to their actions and underscores an urgent need for new studies in this area. The preponderance of the data support the view that discharge arising in slowly adapting pulmonary stretch receptors plays an important role in the initiation of the widespread and highly coordinated recruitment of laryngeal, tongue, and hyoid muscles during airway obstruction.


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