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.

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.

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.

Responses of pulmonary stretch receptors during ramp inflations of the lung

1986 ◽  
Vol 61 (1) ◽  
pp. 344-352 ◽  
Author(s):  
A. I. Pack ◽  
M. D. Ogilvie ◽  
R. O. Davies ◽  
R. J. Galante
Keyword(s):  
Transpulmonary Pressure ◽  
Type I ◽  
Single Population ◽  
Lung Inflation ◽  
Lung Expansion ◽  
Constant Rate ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Multiple Levels ◽  
Pulmonary Stretch Receptor

Studies were conducted in anesthetized paralyzed dogs to determine how the dynamic and proportional sensitivity of pulmonary stretch receptors change during lung inflation. The firing of each receptor was examined at multiple levels of static transpulmonary pressure and during multiple identical inflations at each of several rates. The averaged response of the receptor was computed and receptor activity related to transpulmonary pressure. On the basis of a quantitative criterion, employed to distinguish type I from type II receptors, the receptors could not be divided into distinct subpopulations. Thus all receptors were treated as coming from a single population. For all receptors we observed that their proportional sensitivity (increases in firing produced by increases in lung expansion at a constant rate of inflation) declined as the lung was inflated. In contrast, the dynamic sensitivity (increases in firing produced by increased rates of inflation at constant transpulmonary pressure) increased or remained relatively constant with increasing lung expansion. Thus, as inflation volume increases, the pulmonary stretch receptor acts increasingly as a rate receptor. The rate of inflation may have a more important role in control of the inspiratory duration than previously realized.

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.

High lung volume increases stress failure in pulmonary capillaries

1992 ◽  
Vol 73 (1) ◽  
pp. 123-133 ◽  
Author(s):  
Z. Fu ◽  
M. L. Costello ◽  
K. Tsukimoto ◽  
R. Prediletto ◽  
A. R. Elliott ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Lung Volume ◽  
Autologous Blood ◽  
Physiological Mechanism ◽  
Transpulmonary Pressure ◽  
Lung Volumes ◽  
Lung Inflation ◽  
Pulmonary Capillaries ◽  
Scanning Electron

We previously showed that when pulmonary capillaries in anesthetized rabbits are exposed to a transmural pressure (Ptm) of approximately 40 mmHg, stress failure of the walls occurs with disruption of the capillary endothelium, alveolar epithelium, or sometimes all layers. The present study was designed to test whether stress failure occurred more frequently at high than at low lung volumes for the same Ptm. Lungs of anesthetized rabbits were inflated to a transpulmonary pressure of 20 cmH2O, perfused with autologous blood at 32.5 or 2.5 cmH2O Ptm, and fixed by intravascular perfusion. Samples were examined by both transmission and scanning electron microscopy. The results were compared with those of a previous study in which the lung was inflated to a transpulmonary pressure of 5 cmH2O. There was a large increase in the frequency of stress failure of the capillary walls at the higher lung volume. For example, at 32.5 cmH2O Ptm, the number of endothelial breaks per millimeter cell lining was 7.1 +/- 2.2 at the high lung volume compared with 0.7 +/- 0.4 at the low lung volume. The corresponding values for epithelium were 8.5 +/- 1.6 and 0.9 +/- 0.6. Both differences were significant (P less than 0.05). At 52.5 cmH2O Ptm, the results for endothelium were 20.7 +/- 7.6 (high volume) and 7.1 +/- 2.1 (low volume), and the corresponding results for epithelium were 32.8 +/- 11.9 and 11.4 +/- 3.7. At 32.5 cmH2O Ptm, the thickness of the blood-gas barrier was greater at the higher lung volume, consistent with the development of more interstitial edema. Ballooning of the epithelium caused by accumulation of edema fluid between the epithelial cell and its basement membrane was seen at 32.5 and 52.5 cmH2O Ptm. At high lung volume, the breaks tended to be narrower and fewer were oriented perpendicular to the axis of the pulmonary capillaries than at low lung volumes. Transmission and scanning electron microscopy measurements agreed well. Our findings provide a physiological mechanism for other studies showing increased capillary permeability at high states of lung inflation.

Connectivity of slowly adapting pulmonary stretch receptors with dorsal medullary respiratory neurons

1987 ◽  
Vol 58 (6) ◽  
pp. 1259-1274 ◽  
Author(s):  
A. J. Berger ◽  
T. E. Dick
Keyword(s):  
Electrical Stimulation ◽  
Membrane Potential ◽  
Beta Cells ◽  
Spike Activity ◽  
Alpha Cells ◽  
Drg Neurons ◽  
Lung Inflation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
P Cells

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.

Trapped air in ventilated excised rat lungs

1976 ◽  
Vol 40 (6) ◽  
pp. 915-922 ◽  
Author(s):  
D. G. Frazer ◽  
K. C. Weber
Keyword(s):  
Stress Relaxation ◽  
Flow Rate ◽  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Maximum Pressure ◽  
Lung Inflation ◽  
Minimum Pressure ◽  
Trapped Air ◽  
Rat Lungs ◽  
Reference Pressure

Degassed excised rat lungs were ventilated in a water-filled plethysmograph with the carina as the zero pressure reference. Pressure-volume curves were recorded from a minimum transpulmonary pressure (Pmin) of -5 cmH2O to a maximum pressure (Pmin) of 30 cmH2O. An index of the minimun volume for the lung (Vm) divided by the maximum lung volume for the same cycle (Vmax) was used as an index of the amount of air trapped within the lung. As the flow rate was decreased from 38.2 to 1.9 ml/min, there were significant increases in the amount of air trapped in the lung. As the maximum pressure was decreased to 25 and 20 cmH2O, or the minimum pressure was increased to 6 and 11 cmH2O, the amount of trapped air in the lung significantly decreased. The rate of lung inflation had a much greater influence on the amount of trapped air than either the deflation rate or stress relaxation. The results are consistent with the theory that bubbles are formed during inflation and are the main cause of air trapped in the excised lung.

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.

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