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.

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.

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.

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.

Responses of conscious rabbits to CO2 at ambient temperatures of 5, 20, and 35 degrees C

1979 ◽  
Vol 47 (3) ◽  
pp. 522-526 ◽  
Author(s):  
M. Maskrey ◽  
S. C. Nicol
Keyword(s):  
Body Temperature ◽  
Brain Stem ◽  
Minute Volume ◽  
Atmospheric Air ◽  
Co2 Partial Pressure ◽  
Ambient Temperatures ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Conscious Rabbits ◽  
The Brain

Conscious rabbits were exposed to atmospheric air or to 6% CO2 in air at ambient temperatures (Ta) of 5, 20 and 35 degrees C. Measurements were made of rectal temperature (Tre), metabolic rate (MR), respiratory frequency (f), tidal volume (VT), and minute volume (VE). CO2 exposure did not affect Tre at any Ta and only affected MR at 35 degrees C when it caused an increase. At each Ta hypercapnia caused an increase in VT and a decrease in f. At 5 degrees C VE was increased by CO2, at 35 degrees C VE decreased, and at 20 degrees C the results were variable. The data were examined in the light of theories relating to the relative contributions of inputs from brain stem and from pulmonary stretch receptors, in response to body temperature and CO2 partial pressure. It was concluded that hypercapnia stimulates an increase in VT via the brain stem, whereas at the same time removing a hypocapnic drive which, along with central thermal inputs, stimulates f.

Effect of pulmonary arterial PCO2 on slowly adapting pulmonary stretch receptors

1986 ◽  
Vol 60 (6) ◽  
pp. 2048-2055 ◽  
Author(s):  
J. F. Green ◽  
E. R. Schertel ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Lung Mechanics ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Venous Pco2 ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Right Heart Bypass ◽  
Pulmonary Stretch Receptor

We recorded pulmonary stretch receptor (PSR) activity in anesthetized dogs and examined the effect of varying pulmonary arterial PCO2 (PpCO2) in both the naturally perfused and vascularly isolated pulmonary circulations while ventilating the lungs with room air. Steady-state increases in PpCO2 from approximately 25 to 50 Torr and from 50 to 70 Torr decreased PSR activity (impulses/ventilatory cycle) by 15 and 9%, respectively (P less than 0.001). Rapid increases in PpCO2 from approximately 50 to 80 Torr in a right-heart bypass preparation (with pulmonary blood flow constant) decreased PSR activity by 27%. Depression of firing, which was proportionately greater in deflation, was not dependent on changes in lung mechanics. Results show that loading CO2 intravascularly depresses PSR activity, the effects extending above as well as below resting PpCO2. Rapidly increasing PpCO2 above the resting level markedly depresses PSR activity during the transient. We conclude that PSRs may contribute to altered breathing resulting from changes in mixed venous PCO2 over the physiological range.

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.

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.

Hypoxia potentiates, oxygen attenuates deflation-induced reflex tracheal constriction

1985 ◽  
Vol 59 (3) ◽  
pp. 941-946 ◽  
Author(s):  
E. H. Vidruk
Keyword(s):  
Carotid Body ◽  
Stretch Receptor ◽  
Partial Denervation ◽  
Bilateral Carotid ◽  
Lung Deflation ◽  
Pulmonary Stretch Receptor ◽  
Carotid Body Denervation

The reflex tracheomotor responses of in situ isolated segments of the extrathoracic trachea of anesthetized, paralyzed, and ventilated dogs were monitored. Reflex tracheal constriction was evoked by passive lung deflation. The purpose of this study was to determine whether the prevailing state of oxygenation altered the magnitude of this reflex. Compared with the magnitude of the response during normoxia [arterial O2 tension (PaO2) = 78 Torr], that during hypoxia (PaO2 = 44 Torr) was nearly threefold larger while that during hyperoxia (PaO2 greater than 250 Torr) was about 50% smaller. The isocapnic changes in oxygenation by themselves usually had no effect on tracheomotor tone. The deflation-induced reflex tracheal constriction was eliminated by complete denervation of the tracheal segment but usually only diminished by partial denervation. Bilateral vagotomies or bilateral carotid body denervation also usually decreased the magnitude of the reflex. It appears that the magnitude of this reflex is dependent on the prevailing state of oxygenation and that a pulmonary stretch receptor-carotid body chemoreceptor interaction accounts for the exaggerated reflex tracheal constriction during hypoxia and the attenuated response during hyperoxia.

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.

Effects of skeletal muscle fiber deformation on lymphatic volumes

1990 ◽  
Vol 259 (6) ◽  
pp. H1860-H1868 ◽  
Author(s):  
M. C. Mazzoni ◽  
T. C. Skalak ◽  
G. W. Schmid-Schonbein
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Lymphatic Vessels ◽  
Underlying Mechanism ◽  
Surrounding Tissue ◽  
Cross Sectional ◽  
In Situ Preparation ◽  
Muscle Fascia

Because lymphatics in skeletal muscle have no smooth muscle, they are expanded and compressed solely by stresses in the surrounding tissue. Whole organ experiments have indicated that lymph flow is significantly elevated during muscle activity, yet the underlying mechanism for lymph formation has not been identified. To investigate this mechanism, specimens of the rat spinotrapezius muscle were fixed in situ at the undeformed in vivo length, and also in the stretched and contracted states, for histological examination. Cross-sectional areas of lymphatic vessels, skeletal muscle fibers, blood vessels, and interstitial space were measured using a stereological technique. The in situ preparation with intact muscle fascia was essential for preservation of interstitial volume. The lymphatic cross-sectional areas and muscle stretch ratios from 20 rats showed that lymphatic volume increased by 57% for a 20% stretch, and decreased by 45% for a 20% contraction. Deformation of the incompressible muscle fibers appears to inversely affect surrounding tissue structures; e.g., decreased fiber cross-sectional area during stretch increases interstitial spacing between fibers, which in turn expands lymphatics.

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