Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Pulmonary Stretch Receptors”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1994

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

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.

Airway Resistance↗
PubMed1988

Stimulation of rapidly adapting pulmonary stretch receptors by pulmonary lymphatic obstruction in dogs.

The effects of pulmonary lymphatic obstruction and pulmonary venous congestion on the activities of slowly adapting receptors (SAR) and rapidly adapting receptors (RAR) of the airways were examined in anaesthetized, artificially ventilated dogs. In 11 out of 12 RAR (12 dogs) examined, pulmonary lymphatic obstruction for a period of 20 min produced a sustained significant increase in activity without a significant change in peak airway pressure and dynamic compliance. The activity remained significantly elevated even after the pulmonary lymphatic obstruction was released. This stimulus was without effect on the SAR (n = 5 dogs). Pulmonary venous congestion alone increased the RAR activity (n = 7 dogs) significantly without producing significant changes in airway mechanics. Lymphatic obstruction, when superimposed upon congestion, did not produce a further significant increase in activity. In four dogs the effect of pulmonary venous congestion (left atrial pressure increased from 7.6 +/- 1.7 to 16.3 +/- 2.7 mmHg) (1 mmHg = 133.3 Pa) on pulmonary lymphatic flow was examined. The procedure caused a significant increase in lymph flow. These results suggest that in the dog, the RAR activity is influenced by changes in the pulmonary extravascular space.

Adaptation, Physiological↗
PubMed1986

Effect of pulmonary arterial PCO2 on slowly adapting pulmonary stretch receptors.

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.

Adaptation, Physiological↗
PubMed1986

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

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.

Action Potentials↗
PubMed1983

Within-breath PCO2 levels in the airways and at the pulmonary stretch receptor sites.

The discharge frequency of pulmonary stretch receptors (PSRs) shows an inverse responsiveness to the CO2 partial pressure (PCO2), which is limited to an extremely hypocapnic range. During inspiration extremely hypocapnic PCO2 levels are obtained in a large part of the respiratory tract due to the diffusion limited gas mixing. The question remains whether PSRs in combination with these low levels of PCO2 are involved in the regulation of breathing. As a necessary first step to be able to answer this question, this paper is devoted to the calculation of the within-breath PCO2 transients in the respiratory tract and the corresponding PCO2 oscillations in the superficial airway tissue. For PSRs located in the smooth muscles of large bronchi, the calculations predict a time delay of a few seconds to adapt their discharge frequency to a change in PCO2 in the airway lumen. The result is in good agreement with the observed time delay reported in the literature. For the PSRs located in the acini the calculated time constant of their discharge response to PCO2 variations in the lumen is much smaller than 250 ms. This implies a within-breath response to the oscillating luminal PCO2. Further, the calculations show that a CO2 diffusion front is established within the acini during early inspiration. This diffusion front penetrates further and further into the acini with increasing work load due to the concomitant increase in inspiratory flow. As a consequence, the discharge frequency vs. volume response curve of PSRs, especially those located in distal airways, may be modified by a flow-induced PCO2-related contribution.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteries↗
PubMed1983

Projection of single pulmonary stretch receptors to solitary tract region.

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.

Action Potentials↗
PubMed1984

Modulation of pulmonary stretch receptors and airway resistance by parasympathetic efferents.

Recording from pulmonary stretch receptors in the intact cervical vagus nerve revealed a novel interaction between stretch receptors and smooth muscle in the lungs of anesthetized paralyzed cats. Firing rates of pulmonary stretch receptors were modulated in step with the inflation-deflation cycle of the mechanical respirator, as expected. Firing rates of most slowly adapting receptors, but not rapidly adapting receptors, were also strongly modulated in step with the phrenic nerve activity even when the respirator was turned off and the cat motionless. The modulation of some receptors' firing rates by the inspiratory motor output was as great as the change in firing-rate in response to a lung inflation of 20 ml of air (one tidal volume). Atropine blocked the inspiratory-related modulation of slowly adapting/receptor firing rates; it did not block the inflation-related modulation. Pulmonary resistance was modulated in step with the inspiratory activity on the phrenic nerve. Hyperventilation to neural apnea (no phrenic nerve activity) reduced pulmonary resistance to its lowest level, a level equal to that produced by an injection of isoproterenol or atropine. Hypoxia during hypocapnic apnea caused bursts of inspiratory activity on the phrenic nerve accompanied by one-to-one increases in airway resistance. We conclude that the intrathoracic airway smooth muscle contracts with each neural inspiration, that the modulation of the pulmonary stretch receptors is due to a mechanical interaction with the intrathoracic airway smooth muscle, and that through the mechanical link with airway smooth muscle, stretch receptor sensitivity depends on inspiratory output, a closed loop.

Afferent Pathways↗
PubMed1992

Cholinergic and H1-receptor influences of histamine on slowly adapting pulmonary stretch receptor activity in the rabbit.

Afferent impulses of slowly adapting pulmonary stretch receptors (SARs) were obtained by dissecting fine slips from the left vagus nerve (LVN) and by leaving the rest of the nerve intact. In the same SAR preparation, changes of the receptor activity in response to right atrial injections of histamine (10 and 60 micrograms/kg) were successively examined before and after atropine (1 mg/kg), partial vagal efferent ablation, and mequitazine (1 mg/kg) in 10 rabbits. Administration of histamine led to an increase in the SAR activity, and this effect became more pronounced by increasing the dose of histamine. Atropine treatment diminished the responses of SARs to histamine at different doses. Partial vagal efferent ablation produced by denervation of the rest of the intact LVN slightly reduced the response of SARs to histamine at 10 micrograms/kg but had no significant effect on the SAR response to 60 micrograms/kg histamine. In the absence of vagal afferent and efferent activities on the left side, mequitazine, a potent H1-receptor blocker, completely blocked low- and high-dose effects of histamine on SARs. We compared the responses of the receptor activity to aerosol histamine (1 and 4%) and to topical application of histamine (0.1 ml, 0.025% and 0.1%) in six SAR preparations. The magnitude and duration of increased SAR activity became more prominent by increasing the concentration of histamine. The firing pattern and discharge rate of SARs following aerosol or intratracheal administration of histamine were similar to those after intra-atrial histamine. In addition, we also examined the excitatory responses of SAR activity to right atrial injections of histamine at 10 and 60 micrograms/kg before and after topical administration of atropine (0.1 ml, 1%, n = 6) or mequitazine (0.1 ml, 1%, n = 6) in 12 SAR preparations. Intratracheal atropine diminished the response of SARs to 10 micrograms/kg of histamine but had no significant effect on the response of SARs to histamine at 60 micrograms/kg. All the responses of SARs to histamine were completely blocked by topical application of mequitazine. These results suggest that the change of SAR activity produced by histamine at 10 micrograms/kg occurs mainly as a result of the release of acethylcholine (ACh) via the vagovagal reflex and that the activation of H1-receptors of the airway smooth muscle contributes importantly to the response of SARs to histamine at 60 micrograms/kg.

Acetylcholine↗
PubMed1979

Adaptation of pulmonary stretch receptors in different mammalian species.

A consequence of the adaptation of pulmonary stretch receptors is that their pattern of discharge depends on both lung volume and its rate of change. For adaptation dependent, flow related information to modify the breathing pattern by a feedback process, appreciable receptor adaptation must take place during a single respiratory cycle. Moreover, for flow related information to have the same significance in all animals, the time course of stretch receptor adaptation would have to vary among species, being more rapid in small animals, with high respiratory frequencies. We recorded single fiber action potentials from 84 pulmonary stretch receptors in six species of mammals, ranging from hamster to dog. The response of the receptors to maintained transpulmonary pressures was similar in the different species,as was the time course of receptor adptation following sudden lung inflations to 5 and 10 cm H2O. These findings show that the behavior of pulmonary stretch receptors is similar in animals with widely differing respiratory frequencies, and that the significance of receptor adaptation for regulation of the breathing pattern must vary interspecifically.

Action Potentials↗
PubMed1984

Evidence for a monosynaptic connection between slowly adapting pulmonary stretch receptor afferents and inspiratory beta neurones.

The synaptic connection between slowly adapting pulmonary stretch receptor afferents and inspiratory neurones within a region ventral to the tractus solitarius was determined using intracellular recording and spike triggered averaging techniques. When the vagus nerve was stimulated at intensities eliciting a Hering-Breuer reflex, the difference in mean latency between centrally recorded action potentials of slowly adapting pulmonary stretch receptor afferents and e.p.s.p.s of inspiratory beta neurones was 0.2 ms. This difference is indicative of a monosynaptic connection. Extracellular single unit spikes of slowly adapting pulmonary stretch receptors recorded from the nodose ganglion were used to trigger the averaging of synaptic noise recorded from inspiratory neurones. A prominent wave of synaptic depolarization was observed in all inspiratory beta neurones even when a small number of sweeps were averaged. This depolarization was absent from inspiratory alpha neurones. The shape indices of these depolarizations are consistent with a monosynaptic connection between slowly adapting pulmonary stretch receptor afferents and inspiratory beta neurones. In addition, the data raise the possibility that this connection is multiple and distributed.

Animals↗
PubMed1976

The direct effect on pulmonary stretch receptor discharge produced by changing lung carbon dioxide concentration in dogs on cardiopulmonary bypass and its action on breathing.

1. Single fibre pulmonary stretch receptor discharge was recorded in dogs on cardiopulmonary bypass. 2. Inhalation of CO2 depressed pulmonary stretch receptor discharge despite the absence of changes in arterial PCO2. This effect was particularly marked with airway CO2 levels below 5%. 3. Changing arterial PCO2, without changing airway CO2, had only small and insignificant effects on pulmonary stretch receptor discharge. 4. The effect of changes in airway CO2 on pulmonary stretch receptor discharge was rapid and correlated well in time with the reflex tachypnoea produced when CO2 was inhaled in conditions of cardiopulmonary bypass. 5. Stimulation of the central end of the cut vagus nerve was triggered from simultaneously recorded action potentials from a single pulmonary stretch receptor. 6. In these conditions, the reflex response to CO2 could be simulated provided that the pulmonary stretch receptor had an end-expiratory discharge. 7. It is suggested that the vagally mediated tachypnoeic response to changes in airway CO2 seen in conditions of cardiopulmonary bypass is due to the effect of CO2 on the end-expiratory discharge of pulmonary stretch receptors.

Action Potentials↗
PubMed2005

Ouabain stimulates slowly adapting pulmonary stretch receptors.

Ouabain, a Na(+)/K(+)-ATPase inhibitor, induces slowly adapting pulmonary stretch receptors (SARs) to discharge paradoxically. Paradoxical discharge is characterized by increased SAR activity during lung deflation coupled with silence during lung inflation. We hypothesized that over-excitation silences the SARs. Accordingly, if cyclic inflation pressure was reduced so as to lower SAR stimulation, paradoxical discharge would be prevented. In the present study, single-unit activity of SARs was recorded in anesthetized, open-chest and mechanically ventilated rabbits with positive-end-expiratory pressure (PEEP). After microinjection of ouabain into the receptive field, SAR activity initially increased and then gradually became paradoxical. During paradoxical cycling, SAR activity started and stopped abruptly, oscillating between high frequency discharge during lung deflation and silence during peak inflation. Removing PEEP reduced basal cyclic stimulation and returned the discharge pattern to normal, that is, SAR activity was highest at peak inflation pressure but silent during deflation. It is speculated that stretching SARs causes Na(+) influx, producing generator potential (GP). Normally, GP recovers by Na(+) extrusion via Na(+)/K(+)-ATPase. Ouabain inhibits the ATPase, which limits Na(+) extrusion, and thus sustains the GP. Therefore, after ouabain microinjection, lung inflation will further increase GP, causing over-excitation to silence the SARs.

Action Potentials↗
PubMed1978

[Effect of the dynamic factor on the discharge frequency of high threshold pulmonary stretch receptors in cats].

The discharge frequency of high threshold pulmonary stretch receptor at the end of inspiration is much greater than at the corresponding lung volume under static conditions. During inspiratory phase the discharge frequency of some receptors (type IV) is created by dynamic factor by 90% ("rate" receptors). In static conditions the lowering of discharge frequency of most of the receptors under study makes 9--13% at 10s, though in some receptors (type III)--makes 28% at 10s. Properties of most of the pulmonary stretch receptors under study were changed with increasing of threshold. The frequency of discharges during inspiratory phase or lung inflation becomes lower, the influence of dynamic factor on receptor activity becomes relatively potent, the frequency of discharges vs lung volume ratio becomes different.

Animals↗
PubMed1993

Effects of calcium channel and H1-receptor blockers on the responses of slowly adapting pulmonary stretch receptors to histamine in vagotomized rabbits.

We studied the effects of calcium channel antagonists (verapamil and nifedipine) and H1-receptor blockers (mequitazine) on changes in the slowly adapting pulmonary stretch receptors (SARs) located below the carina in response to right atrial injections of histamine (60 and 80 micrograms/kg) in anesthetized artificially ventilated rabbits with bilateral vagotomy. After histamine was injected into the right atrium, the SARs became more active during expiration but decreased their activity during inspiration. These changes were more pronounced by increasing the dosage of histamine. However, administration of histamine had no significant effect on tracheal pressure (PT). Verapamil treatment (1 mg/kg) did not alter the SAR response to histamine, whereas the responses of SARs to histamine at different dosages were significantly diminished by treatment with nifedipine (1 mg/kg). Mequitazine (1 mg/kg), a potent H1-receptor blocker, blocked completely all the responses of SAR activity to histamine. These results suggest that the effect of histamine 60-80 micrograms/kg on SAR activity is mediated by the activation of H1-receptors of the peripheral airway smooth muscle and that this activation, at least in part, involves the opening of calcium channels of the airway smooth muscle.

Animals↗
PubMed2003

Structure of slowly adapting pulmonary stretch receptors in the lung periphery.

Pulmonary sensory receptors are the initiating sites for lung reflexes; however, little is known about their structure, especially the relationship between the structure and function of these receptors. Using a novel approach (combining electrophysiological and morphological techniques), we examined the structures of the typical slowly adapting pulmonary stretch receptors (SARs) located in the lung periphery. We recorded SAR activities in the cervical vagus nerve, identified the receptive field, dissected the SARs in blocks, fixed and processed these blocks for immunohistochemical staining using anti-Na+/K+-ATPase, and examined the blocks under a confocal microscope. These SAR structures have multiple endings that have terminal knobs. Some structures that are located in the airway walls have terminal knobs buried in smooth muscle. Others are in the most peripheral part of the lung, and their terminal knobs have no obvious relation to smooth muscle, suggesting that muscle contraction may not be a direct factor for SAR activation.

Animals↗