Tonic pulmonary stretch receptor feedback modulates both eupnea and gasping in an in situ rat preparation

2003 ◽  
Vol 285 (1) ◽  
pp. R215-R221 ◽  
Author(s):  
Michael B. Harris ◽  
Walter M. St.-John
Keyword(s):  
Stretch Receptor ◽  
Afferent Feedback ◽  
Lung Inflation ◽  
In Situ Preparation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Discharge Patterns ◽  
Pulmonary Stretch Receptor

The perfused in situ juvenile rat preparation produces phrenic discharge patterns comparable to eupnea and gasping in vivo. These ventilatory patterns of eupnea and gasping differ in multiple aspects, including most prominently the rate of rise of inspiratory activity. Because gasping, but not eupnea, appeared similar after vagotomy in spontaneous breathing preparations, it has been assumed that gasping was unresponsive to afferent stimuli from pulmonary stretch receptors. In the present study, efferent activity of the phrenic nerve was recorded during eupnea and gasping in the in situ juvenile rat preparation. Gasping was induced in hypoxic-hypercapnia or ischemia. An increase in the pressure of tonic lung inflation from 1 to 10 cmH2O caused a prolongation of the duration between phrenic bursts in both eupnea or gasping. Bilateral vagotomy eliminated these changes. We conclude that the neural substrate mediating the Hering-Breuer reflex is retained in the in situ preparation and that the brain stem circuitry generating the respiratory patterns responds to tonic activation of pulmonary stretch receptors in a similar manner in eupnea and gasping. These findings support the homology of eupnea-like phrenic discharge patterns in the reduced in situ preparation and eupnea in vivo and disprove the common supposition that gasping is insensitive to vagal afferent feedback from pulmonary stretch receptor mechanisms.

Phasic pulmonary stretch receptor feedback modulates both eupnea and gasping in an in situ rat preparation

2005 ◽  
Vol 289 (2) ◽  
pp. R450-R455 ◽  
Author(s):  
Michael B. Harris ◽  
Walter M. St.-John
Keyword(s):  
Brain Stem ◽  
Stretch Receptor ◽  
Afferent Feedback ◽  
Burst Frequency ◽  
In Situ Preparation ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Pulmonary Stretch Receptor

The perfused in situ juvenile rat preparation produces patterns of phrenic discharge comparable to eupnea and gasping in vivo. These ventilatory patterns differ in multiple aspects, including most prominently the rate of rise of inspiratory activity. Although we have recently demonstrated that both eupnea and gasping are similarly modulated by a Hering-Breuer expiratory-promoting reflex to tonic pulmonary stretch, it has generally been assumed that gasping was unresponsive to afferent stimuli from pulmonary stretch receptors. In the present study, we recorded eupneic and gasplike efferent activity of the phrenic nerve in the in situ juvenile rat perfused brain stem preparation, with and without phrenic-triggered phasic pulmonary inflation. We tested the hypothesis that phasic pulmonary inflation produces reflex responses in situ akin to those in vivo and that both eupnea and gasping are similarly modulated by phasic pulmonary stretch. In eupnea, we found that phasic pulmonary inflation decreases inspiratory burst duration and the period of expiration, thus increasing burst frequency of the phrenic neurogram. Phasic pulmonary inflation also decreases the duration of expiration and increases the burst frequency during gasping. Bilateral vagotomy eliminated these changes. We conclude that the neural substrate mediating the Hering-Breuer reflex is retained in the in situ preparation and that the brain stem circuitry generating the respiratory patterns respond to phasic activation of pulmonary stretch receptors in both eupnea and gasping. These findings support the homology of eupneic phrenic discharge patterns in the reduced in situ preparation and eupnea in vivo and disprove the common supposition that gasping is insensitive to vagal afferent feedback from pulmonary stretch receptor mechanisms.

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.

scholarly journals Pontine respiratory activity involved in inspiratory/expiratory phase transition

2009 ◽  
Vol 364 (1529) ◽  
pp. 2517-2526 ◽  
Author(s):  
Michael Mörschel ◽  
Mathias Dutschmann
Keyword(s):  
Phase Transition ◽  
Sensory Feedback ◽  
Respiratory Pattern ◽  
Respiratory Neurons ◽  
Related Activity ◽  
Lung Inflation ◽  
Pulmonary Stretch Receptors

Control of the timing of the inspiratory/expiratory (IE) phase transition is a hallmark of respiratory pattern formation. In principle, sensory feedback from pulmonary stretch receptors (Breuer–Hering reflex, BHR) is seen as the major controller for the IE phase transition, while pontine-based control of IE phase transition by both the pontine Kölliker–Fuse nucleus (KF) and parabrachial complex is seen as a secondary or backup mechanism. However, previous studies have shown that the BHR can habituate in vivo . Thus, habituation reduces sensory feedback, so the role of the pons, and specifically the KF, for IE phase transition may increase dramatically. Pontine-mediated control of the IE phase transition is not completely understood. In the present review, we discuss existing models for ponto-medullary interaction that may be involved in the control of inspiratory duration and IE transition. We also present intracellular recordings of pontine respiratory units derived from an in situ intra-arterially perfused brainstem preparation of rats. With the absence of lung inflation, this preparation generates a normal respiratory pattern and many of the recorded pontine units demonstrated phasic respiratory-related activity. The analysis of changes in membrane potentials of pontine respiratory neurons has allowed us to propose a number of pontine-medullary interactions not considered before. The involvement of these putative interactions in pontine-mediated control of IE phase transitions is discussed.

Effect of expiratory loading on expiratory duration and pulmonary stretch receptor discharge

1986 ◽  
Vol 61 (5) ◽  
pp. 1857-1863 ◽  
Author(s):  
P. W. Davenport ◽  
J. A. Wozniak
Keyword(s):  
Linear Relationship ◽  
Temporal Summation ◽  
Spatial Summation ◽  
Stretch Receptor ◽  
Single Breath ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Temporal And Spatial ◽  
Resistive Loads ◽  
Pulmonary Stretch Receptor

Slowly adapting pulmonary stretch receptors have been hypothesized to be the afferents mediating the vagally dependent, volume-related prolongation of expiratory time (TE) during expiratory loading. It has been further suggested that the vagal component of this prolongation of TE is due to the temporal summation of pulmonary stretch receptor (PSR) activity during expiratory loading. This hypothesis was tested in rabbits exposed to resistive and elastic single-breath expiratory loading while PSR′s were simultaneously recorded. Both types of loads resulted in a decreased expired volume (VE) and increased expiratory duration (TE). The TE for resistive loads were significantly greater than for elastic loads for equivalent VE. Thus two different VE-TE relationships were found for resistive and elastic loads. When TE was plotted against the area under the expired volume trajectory, a single linear relationship was observed. PSR activity recorded during expiratory loading increased as VE decreased and TE increased. A single linear relationship resulted when the number of PSR spikes during the expiration was plotted against the associated TE for all types of loads. These findings demonstrate that the volume-related prolongation of TE with single-breath expiratory loads is associated with an increase in PSR discharge. These results support the hypothesis that the vagal component of load-dependent prolongation of TE is a function of both the temporal and spatial summation of PSR activity during the expiratory phase.

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.

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.

Projection of single pulmonary stretch receptors to solitary tract region

1983 ◽  
Vol 49 (3) ◽  
pp. 819-830 ◽  
Author(s):  
A. J. Berger ◽  
D. B. Averill
Keyword(s):  
Transpulmonary Pressure ◽  
Linear Increase ◽  
Stretch Receptor ◽  
Synaptic Potentials ◽  
Medial Nucleus ◽  
Stretch Receptors ◽  
Ventrolateral Nucleus ◽  
Pulmonary Stretch Receptors ◽  
The Difference ◽  
Pulmonary Stretch Receptor

1. Central projections of single slowly adapting pulmonary stretch receptors were mapped in the medulla by the technique of spike-triggered averaging of extracellular field potentials. Discharge of pulmonary stretch receptors was recorded in continuity from the nodose ganglion; this activity provided the trigger for an averaging computer. 2. These pulmonary stretch receptors were characterized by a linear increase in firing rate in response to increases in transpulmonary pressure, an adaptation index, and peripheral axonal and intramedullary conduction velocities. 3. In accordance with the terminology used by Munson and Sypert (21), three types of electrical potentials were observed for the projection of a pulmonary stretch receptor in the medulla. Axonal potentials were recorded when the brain stem electrode was in the vicinity of the afferent axon. Terminal potentials were recorded when the electrode was adjacent to terminations of the afferent axon. Focal synaptic potentials were recorded when the electrode was near postsynaptic units receiving input from the pulmonary stretch receptor. Maxima of terminal potentials were recorded in a region 1 mm rostral to the obex in the medial nucleus of the tractus solitarius (six cases), in the ventrolateral nucleus of the tractus solitarius (three cases), and in an area just dorsolateral to the tractus solitarius (two cases). Focal synaptic potentials for five pulmonary stretch receptors were observed in a region 1 mm rostral to obex. Maxima of these potentials were recorded in the medial nucleus of tractus solitarius (two cases), in the ventrolateral nucleus of tractus solitarius (two cases), and in an area just dorsolateral to the tractus solitarius (one case). 4. Occasionally both terminal and focal synaptic potentials were observed for the same pulmonary afferent. The difference in the latencies of these potentials fell within the range previously reported for monosynaptic connections of muscle spindle Ia and group II afferents for alpha-motoneurons. This suggests that the afferents of pulmonary stretch receptors have monosynaptic connections with neurons in the medial nucleus of the tractus solitarius, in the ventrolateral nucleus of the tractus solitarius, and in an area dorsolateral to the tractus solitarius.

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.

Factors determining degree of inflation in intratracheally fixed rat lungs

1980 ◽  
Vol 48 (2) ◽  
pp. 389-393 ◽  
Author(s):  
G. Hayatdavoudi ◽  
J. D. Crapo ◽  
F. J. Miller ◽  
J. J. O'Neil
Keyword(s):  
Slow Rate ◽  
Total Lung Capacity ◽  
Formaldehyde Solution ◽  
Initial Flow ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Final Degree ◽  
Low Rate

The total lung capacity (TLC) of rats was measured in vivo and was compared to the displacement volume of the lungs following intratracheal fixation with glutaraldehyde or formaldehyde solution. When glutaraldehyde was used the speed of infusion of the fixative was an important factor in the final degree of lung inflation achieved. With a low rate of fixative infusion and a final pressure of 20 cm of fixative the glutaraldehyde-fixed lungs inflated to 55% TLC. With a high initial flow of glutaraldehyde and a final pressure of 20 cm of fixative the lungs inflated to 84% TLC. Fixation of lungs inside the intact chest wall was found to result in a higher degree of inflation. With a reservoir height of 20 cm and a low rate of fixative infusion lungs fixed in situ reached 74% TLC, whereas lungs fixed in situ, but from animals that have been exsanguinated prior to fixation, inflated to only 58% TLC. This suggests that the volume of the blood in the lungs prior to infusion of glutaraldehyde influences the degree of inflation achieved. Formaldehyde-fixed lungs required 72 h to be completely fixed and they were inflated to 90% TLC when a reservoir height of 20 cm was used. Because of the slow rate of fixation using with formaldehyde solution the rate of infusion was found not to limit the degree of inflation that could be achieved.

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