Effect of Volume and Rate of Inflation and Deflation on Transpulmonary Pressure and Response of Pulmonary Stretch Receptors

1956 ◽  
Vol 187 (3) ◽  
pp. 558-566 ◽  
Author(s):  
Harry L. Davis ◽  
Ward S. Fowler ◽  
Edward H. Lambert
Keyword(s):  
Lung Volume ◽  
Action Potentials ◽  
Work Of Breathing ◽  
Transpulmonary Pressure ◽  
Nerve Fibers ◽  
Discharge Frequency ◽  
Afferent Nerve Fibers ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Vagal Afferent

Action potentials of single vagal afferent nerve fibers from slowly adapting pulmonary stretch receptors, transpulmonary pressure and rate of air flow were recorded in anesthetized cats with open thoraxes during varied volumes and rates of inflation and deflation of the lungs. Both discharge frequency and total transpulmonary pressure varied with lung volume and also with its rate and sign of change. Effects of acceleration of volume on discharge frequency were not observed. The receptors provide signals related to the work of breathing.

Lung inflation: effects on heart rate, respiration, and vagal afferent activity in seals

1981 ◽  
Vol 240 (2) ◽  
pp. H190-H198 ◽  
Author(s):  
J. E. Angell-James ◽  
R. Elsner ◽  
M. De Burgh Daly
Keyword(s):  
Transpulmonary Pressure ◽  
Harbor Seal ◽  
Nerve Fibers ◽  
Cardiac Response ◽  
Impulse Frequency ◽  
Lung Inflation ◽  
Afferent Nerve Fibers ◽  
Close Relationship ◽  
Vagal Afferent ◽  
Carotid Body Chemoreceptors

In the anesthetized harbor seal, Phoca vitulina, the Hering-Breuer inflation reflex was weak and comparable to that in humans. Single inflations of the lungs from a syringe during the expiratory phase of normal breathing caused temporary inhibition of breathing and an immediate tachycardia dependent on the integrity of the cervical vagosympathetic nerves. A similar cardiac response occurred when the lungs were artificially inflated during an experimental dive and under conditions in which apnea and bradycardia were reflexly induced by a combination of stimulation of the carotid body chemoreceptors and of the trigeminal or laryngeal input. Recordings from single vagal afferent nerve fibers innervating presumptive pulmonary stretch receptors showed a close relationship between the increase in impulse frequency and increase in lung volume or transpulmonary pressure. It appears that in diving the decrease in pulmonary stretch receptor activity during apnea, combined with cessation of central inspiratory neuronal drive, is an important integrative mechanism that helps development of the reflex bradycardia of trigeminal, carotid, chemoreceptor, and baroreceptor origin.

Hering–Breuer inflation reflex in young and adult mammals

1981 ◽  
Vol 59 (9) ◽  
pp. 1017-1021 ◽  
Author(s):  
C. Gaultier ◽  
J. P. Mortola
Keyword(s):  
Mechanical Properties ◽  
Respiratory System ◽  
Lung Volume ◽  
Young Animal ◽  
Transpulmonary Pressure ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Chemical Stimuli ◽  
Underlying Mechanisms

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.

Effect of central CO2 drive on lung inflation responses of expiratory bulbospinal neurons in dogs

2000 ◽  
Vol 279 (5) ◽  
pp. R1606-R1618 ◽  
Author(s):  
Mislav Tonkovic-Capin ◽  
Edward J. Zuperku ◽  
Eckehard A. Stuth ◽  
Jurica Bajic ◽  
Zoran Dogas ◽  
...  
Keyword(s):  
Empirical Model ◽  
Time Course ◽  
Transpulmonary Pressure ◽  
Neuronal Responses ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Thiopental Sodium ◽  
Inhibitory Components ◽  
Discharge Patterns

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.

Effects of pulmonary air embolism on discharge of slowly adapting pulmonary stretch receptors

1994 ◽  
Vol 76 (1) ◽  
pp. 97-103 ◽  
Author(s):  
B. P. Lee ◽  
H. F. Chen ◽  
F. C. Hsu ◽  
T. B. Kuo ◽  
M. H. Yang
Keyword(s):  
Fiber Type ◽  
Air Embolism ◽  
Transpulmonary Pressure ◽  
Lung Compliance ◽  
Group I ◽  
Airway Collapse ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Close Relationship ◽  
Dynamic Lung Compliance

Pulmonary air embolism (PAE) usually causes small-airway collapse. Local transpulmonary pressure (Ptr) is thought to be closely associated with the activity of slowly adapting pulmonary stretch receptors (SAPSRs). To test whether discharge of SAPSRs located distal to collapsed airways is closely related to the overall Ptr, we studied 65 SAPSRs in anesthetized paralyzed open-chest dogs that were ventilated at constant tidal volume and frequency. PAE increased both Ptr and total pulmonary resistance but decreased dynamic lung compliance. Three groups of SAPSRs were identified on the basis of their locations in intrapulmonary airways. Group I had 29 SAPSRs located in airways < 1 mm in diameter. Group II had 10 SAPSRs that were found in intrapulmonary airways between 1 and 2 mm in diameter. PAE decreased the activity of 31 of the 39 SAPSRs in these two groups. Their activity during PAE was not related to Ptr. The 26 SAPSRs in group III were in airways > 2 mm in diameter. PAE increased the peak firing rate of 18 of these receptors, and there was a close relationship between the discharge frequency of these SAPSRs and the Ptr during PAE. In groups I and II, the dissociation between Ptr and SAPSR activity during PAE may have been caused by peripheral airway collapse. Activity of central fibers was blocked at higher temperatures than activity of peripheral fibers. We suggest that the response of a SAPSR to PAE depends on the location of the receptor within the lungs, and we speculate that threshold and fiber type are also related to location.

Regulation of frequency and depth of breathing during expiratory threshold loading in cats

1975 ◽  
Vol 38 (5) ◽  
pp. 869-874 ◽  
Author(s):  
M. M. Grunstein ◽  
I. Wyszogrodski ◽  
J. Milic-Emili
Keyword(s):  
Tidal Volume ◽  
Lung Volume ◽  
The Other ◽  
Spontaneous Ventilation ◽  
Volume Changes ◽  
Phasic Component ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
The Absolute ◽  
Spontaneously Breathing

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.

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
Keyword(s):  
Lung Volume ◽  
Dynamic Properties ◽  
Constant Flow ◽  
Afferent Activity ◽  
Volume Changes ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Integrative Processing ◽  
Inhibitory Threshold

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.

Pulmonary stretch receptor discharge patterns in eupnea, hypercapnia, and hypoxia

1982 ◽  
Vol 53 (2) ◽  
pp. 346-354 ◽  
Author(s):  
S. Iscoe
Keyword(s):  
Tidal Volume ◽  
Linear Equations ◽  
Discharge Frequency ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Residual Capacity ◽  
Instantaneous Discharge ◽  
Discharge Patterns ◽  
Spontaneously Breathing ◽  
Pulmonary Stretch Receptor

The discharge properties of pulmonary stretch receptors (PSR) were studied in spontaneously breathing, pentobarbital sodium-anesthetized cats. During eupneic breathing, 105 of 116 PSR (both tonically and phasically active) were recruited in the first third of inspiration; none were recruited in the last third. Linear equations adequately expressed the relation between instantaneous discharge frequency and inspired volume in eupnea. During CO2 rebreathing, both tidal volume and peak PSR discharge frequency were inversely related to inspiratory duration. At fixed volumes less than 40 ml above functional residual capacity, instantaneous PSR discharge frequency either did not change or decreased with increases in flow. Above 40 ml, increases in discharge frequency accompanied increases in flow (0.033 spikes/s per ml/s). During progressive hypocapnic hypoxia, discharge frequency increased, on average, at all volumes with increases in flow (0.206 spikes/s per ml/s). During both conditions, as with eupnea, increases in frequency were linearly related to increments in tidal volume. Therefore, tidal volume alone can be used to estimate PSR feedback to the respiratory centers, provided that its instantaneous value is appropriately scaled to account for the different effects of CO2 and hypocapnic hypoxia on PSR discharge.

Reductions of neural activities to upper airway muscles after elevations in static lung volume

1992 ◽  
Vol 73 (2) ◽  
pp. 701-707 ◽  
Author(s):  
W. M. St John ◽  
D. Zhou
Keyword(s):  
Lung Volume ◽  
Cranial Nerve ◽  
Cranial Nerves ◽  
Upper Airway ◽  
Airway Patency ◽  
Reflex Mechanism ◽  
Lung Inflation ◽  
Tracheal Pressure ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

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.

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