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.

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.

scholarly journals Volume-timing relationships during cough and resistive loading in the cat

2000 ◽  
Vol 89 (2) ◽  
pp. 785-790 ◽  
Author(s):  
Donald C. Bolser ◽  
Paul W. Davenport
Keyword(s):  
Linear Relationship ◽  
Negative Slope ◽  
Inspiratory Time ◽  
Positive Slope ◽  
Single Breath ◽  
Resistive Loading ◽  
Resistive Loads ◽  
The Relationship ◽  
Pattern Regulation ◽  
Pulmonary Volume

The relationship between pulmonary volume-related feedback and inspiratory (CTi) and expiratory (CTe) phase durations during cough was determined. Cough was produced in anesthetized cats by mechanical stimulation of the intrathoracic tracheal lumen. During eupnea, the animals were exposed to single-breath inspiratory and expiratory resistive loads. Cough was associated with large increases in inspiratory volume (Vi) and expiratory volume (Ve) but no change in phase durations compared with eupnea. There was no relationship between Viand CTi during coughing. A linear relationship with a negative slope existed between Vi and eupneic inspiratory time during control and inspiratory resistive loading trials. There was no relationship between Ve and CTe during all coughs. However, when the first cough in a series or a single cough was analyzed, the Ve/CTe relationship had a positive slope. A linear relationship with a negative slope existed between Ve and eupneic expiratory time during control and expiratory resistive loading trials. These results support separate ventilatory pattern regulation during cough that does not include modulation of phase durations by pulmonary volume-related feedback.

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.

Central integration of pulmonary stretch receptor input in the control of expiration

1982 ◽  
Vol 52 (5) ◽  
pp. 1296-1315 ◽  
Author(s):  
E. J. Zuperku ◽  
F. A. Hopp ◽  
J. P. Kampine
Keyword(s):  
Temporal Summation ◽  
Stretch Receptor ◽  
Common Mechanism ◽  
Central Processing ◽  
Long Time ◽  
Residual Capacity ◽  
Receptor Input ◽  
Discharge Patterns ◽  
Lung Deflation ◽  
Pulmonary Stretch Receptor

The dynamics of the central processing of the discharge pattern from vagal pulmonary afferents that mediate the expiratory facilitatory reflex have been investigated. These studies involved the development of mathematical models based on analogs of neurophysiological principles such as temporal summation and threshold crossing. These models, which are capable of predicting the expiratory duration for arbitrary discharge patterns, were verified through comparison of their prediction with experimentally obtained relationships between expiratory duration (TE) and waveform parameters of various input patterns. These relationships were obtained by electrical activation of the largest vagal afferent fibers in bilaterally vagotomized, pentobarbital-anesthetized dogs. A parallel two-component model with long time constants (ca. 0.8 and 18 s) was best able to describe the experimental responses. This model suggests that 1) central integration of pulmonary stretch receptor (PSR) input is similar to long time-constant temporal summation; 2) central inspiratory inhibition (no vagal input) may share a common mechanism with vagal processing; 3) PSR-induced inhibition is a linear function of discharge frequency; and 4) TE depends on both the trajectory of lung deflation and the tonic activity at functional residual capacity. These characteristics embody information regarding specific neural arrangements and properties within the respiratory centers.

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.

scholarly journals TEMPORAL SUMMATION IN RHYTHMICALLY ACTIVE MONOSYNAPTIC REFLEX PATHWAYS

1957 ◽  
Vol 40 (3) ◽  
pp. 427-434 ◽  
Author(s):  
David P. C. Lloyd
Keyword(s):  
Temporal Summation ◽  
Spatial Summation ◽  
Monosynaptic Reflex ◽  
Reflex Response ◽  
Frequency Range ◽  
Stimulus Interval ◽  
Reflex Pathways ◽  
Temporal Course ◽  
Fundamental Process ◽  
Temporal And Spatial

Monosynaptic reflex responses elicited by repetitive stimulation in the frequency range between 60 and 100 per second yield evidence of temporal summation. The relation between stimulus interval and mean monosynaptic reflex response in the steady state at the frequencies studied is described adequately by an exponential decaying to 1/e in 4 msec. Since the temporal course of spatial summation is described adequately by the same exponential it is concluded that the two phenomena, temporal and spatial, are expressions of the same fundamental process intrinsic to the workings of the monosynaptic reflex pathway, to wit the synaptic potential-residual facilitation mechanism of prior descriptions. Some discussion of implications is appended.

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