Acute inhalation of ozone stimulates bronchial C-fibers and rapidly adapting receptors in dogs

1993 ◽  
Vol 74 (5) ◽  
pp. 2345-2352 ◽  
Author(s):  
J. C. Coleridge ◽  
H. M. Coleridge ◽  
E. S. Schelegle ◽  
J. F. Green
Keyword(s):  
Lung Compliance ◽  
Acute Exposure ◽  
Ozone Exposure ◽  
C Fibers ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Lower Trachea ◽  
Afferent Response ◽  
Vagal Cooling ◽  
Stimulation Of

To identify the afferents responsible for initiating the vagally mediated respiratory changes evoked by acute exposure to ozone, we recorded vagal impulses in anesthetized, open-chest, artificially ventilated dogs and examined the pulmonary afferent response to ozone (2–3 ppm in air) delivered to the lower trachea for 20–60 min. Bronchial C-fibers (BrCs) were the lung afferents most susceptible to ozone, the activity of 10 of 11 BrCs increasing from 0.2 +/- 0.2 to 4.6 +/- 1.3 impulses/s within 1–7 min of ozone exposure. Ten of 15 rapidly adapting receptors (RARs) were stimulated by ozone, their activity increasing from 1.5 +/- 0.4 to 4.7 +/- 0.7 impulses/s. Stimulation of RARs (but not of BrCs) appeared secondary to the ozone-induced reduction of lung compliance because it was abolished by hyperinflation of the lungs. Ozone had little effect on pulmonary C-fibers or slowly adapting pulmonary stretch receptors. Our results suggest that both BrCs and RARs contribute to the tachypnea and bronchoconstriction evoked by acute exposure to ozone when vagal conduction is intact and that BrCs alone are responsible for the vagally mediated tachypnea that survives vagal cooling to 7 degrees C.

Pulmonary rapidly adapting receptors reflexly increase airway secretion in dogs

1989 ◽  
Vol 67 (2) ◽  
pp. 682-687 ◽  
Author(s):  
J. Yu ◽  
H. D. Schultz ◽  
J. Goodman ◽  
J. C. Coleridge ◽  
H. M. Coleridge ◽  
...  
Keyword(s):  
Lung Compliance ◽  
Base Line ◽  
Lung Collapse ◽  
C Fibers ◽  
Airway Secretion ◽  
Stretch Receptors ◽  
Dynamic Lung Compliance ◽  
Vagal Cooling ◽  
Tracheal Secretion ◽  
Stimulation Of

We attempted to determine whether stimulation of pulmonary rapidly adapting receptors (RARs) increase tracheal submucosal gland secretion in anesthetized open-chest dogs. Electroneurographic studies of pulmonary afferents established that RARs but not lung C-fibers were stimulated by intermittent lung collapse during deflation, collapse being produced by removing positive end-expiratory pressure (PEEP, 4 cmH2O) or by applying negative end-expiratory pressure (NEEP, -4 cmH2O). We measured tracheal secretion by the “hillocks” method. Removing PEEP or applying NEEP for 1 min increased secretion from a base line of 6.0 +/- 1.1 to 11.8 +/- 1.7 and 22.0 +/- 2.8 hillocks.cm-2.min-1, respectively (P less than 0.005). After PEEP was restored, dynamic lung compliance (Cdyn) was 37% below control, and secretion remained elevated (P less than 0.05). A decrease in Cdyn stimulates RARs but not other pulmonary afferents. Hyperinflation, which restored Cdyn and RAR activity to control, returned secretion rate to base line. Secretory responses to lung collapse were abolished by vagal cooling (6 degrees C), by pulmonary vagal section, or by atropine. We conclude that RAR stimulation reflexly increases airway secretion. We cannot exclude the possibility that reduced input from slowly adapting stretch receptors contributed to the secretory response.

Multireceptor activation of the pulmonary chemoreflex

1991 ◽  
Vol 70 (1) ◽  
pp. 368-370 ◽  
Author(s):  
E. B. Strong ◽  
J. F. Green
Keyword(s):  
Breathing Pattern ◽  
Right Atrial ◽  
Direct Stimulation ◽  
C Fibers ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Shallow Breathing ◽  
Rapid Shallow Breathing ◽  
Stimulation Of ◽  
Secondary Stimulation

Schertel et al. (J. Appl. Physiol. 61: 1237–1240, 1984) reported that pulmonary C fibers initiate the prompt apnea followed by rapid shallow breathing evoked by pulmonary arterial injections of capsaicin. However, doubt has remained as to whether these changes in breathing pattern are induced exclusively by direct stimulation of pulmonary C fibers or whether secondary stimulation of slowly adapting pulmonary stretch receptors by capsaicin-induced reflex bronchoconstriction also contributes to the response. To determine the contribution of this secondary mechanism to changes in breathing pattern, we evoked the pulmonary chemoreflex in spontaneously breathing dogs before and after blockade of muscarinic receptors with atropine. Right atrial injections of capsaicin before the administration of atropine induced a classical pulmonary chemoreflex, i.e., apnea, hypotension, and bradycardia followed by rapid shallow breathing and bronchoconstriction. After atropine, all components of the pulmonary chemoreflex induced by right atrial injections of capsaicin remained intact except bronchoconstriction. However, the absolute magnitude of the change in each component of the reflex except apnea was significantly attenuated. We conclude that the classic pulmonary chemoreflex is a complex phenomenon initiated primarily by stimulation of pulmonary C fibers but significantly influenced by secondary stimulation of slowly adapting pulmonary stretch receptors.

Cigarette smoke in lungs evokes reflex increase in tracheal submucosal gland secretion in dogs

1991 ◽  
Vol 71 (3) ◽  
pp. 900-909 ◽  
Author(s):  
H. D. Schultz ◽  
B. Davis ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Cigarette Smoke ◽  
Lung Compliance ◽  
Vagal Afferents ◽  
Gland Secretion ◽  
Submucosal Gland ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Lower Trachea ◽  
Stimulation Of

Stimulation of pulmonary C-fibers (PCs) by capsaicin and of rapidly adapting receptors (RARs) by reduced lung compliance reflexly increases airway submucosal gland secretion in dogs. Because both PCs and RARs are stimulated by cigarette smoke (nicotine being the primary stimulus), we performed experiments in anesthetized open-chest artificially ventilated dogs (with aortic nerves cut) to determine whether cigarette smoke reflexly stimulates airway secretion. We measured submucosal gland secretion by counting the hillocks in a 1.2-cm2 field of tracheal epithelium coated with tantalum dust. Secretion was stimulated by delivery of 40–320 ml smoke from high-nicotine cigarettes to the lower trachea, secretion rate increasing from 7.4 +/- 1.3 to 48.1 +/- 5.1 hillocks.cm-2.min-1. Results of cutting the pulmonary vagal branches or carotid sinus nerves or both indicated that the secretory response was initiated by stimulation of lower respiratory vagal afferents and augmented several seconds later by stimulation of carotid chemoreceptors. Results of cooling the cervical vagus nerves to 7 and 0 degrees C indicated that most of the vagally mediated increase in secretion was due to stimulation of afferent lung C-fibers.

Surfactant replacement partially restores the activity of pulmonary stretch receptors in surfactant-depleted cats

2006 ◽  
Vol 100 (2) ◽  
pp. 594-601 ◽  
Author(s):  
Richard Sindelar ◽  
Anders Jonzon ◽  
Andreas Schulze ◽  
Gunnar Sedin
Keyword(s):  
Respiratory Rate ◽  
Spontaneous Breathing ◽  
Lung Lavage ◽  
Lung Compliance ◽  
High Threshold ◽  
Inspiratory Time ◽  
Impulse Frequency ◽  
Surfactant Replacement ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors

Single units of slowly adapting pulmonary stretch receptors (PSRs) were investigated in anesthetized cats during spontaneous breathing on continuous positive airway pressure (2–5 cmH2O), before and after lung lavage and then after instillation of surfactant to determine the PSR response to surfactant replacement. PSRs were classified as high threshold (HT) and low threshold (LT), and their instantaneous impulse frequency ( fimp) was related to transpulmonary pressure (Ptp) and tidal volume (Vt). Both the total number of impulses and maximal fimp of HT and LT PSRs decreased after lung lavage (55 and 45%, respectively) in the presence of increased Ptp and decreased Vt. While Ptp decreased markedly and Vt remained unchanged after surfactant instillation, all except one PSR responded with increased total number of impulses and maximal fimp (42 and 26%, respectively). Some HT PSRs ceased to discharge after lung lavage but recovered after surfactant instillation. The end-expiratory activity of LT PSRs increased or was regained after surfactant instillation. After instillation of surfactant, respiratory rate increased further with a shorter inspiratory time, resulting in a lower inspiratory-to-expiratory time ratio. Arterial pH decreased (7.31 ± 0.04 vs. 7.22 ± 0.06) and Pco2 increased (5.5 ± 0.7 vs. 7.2 ± 1.3 kPa) after lung lavage, but they were the same after as before instillation of surfactant (pH = 7.21 ± 0.08 and Pco2 = 7.6 ± 1.4 kPa) during spontaneous breathing. In conclusion, surfactant instillation increased lung compliance, which, in turn, increased the activity of both HT and LT PSRs. A further increase in respiratory rate due to a shorter inspiratory time after surfactant instillation suggests that the partially restored PSR activity after surfactant instillation affected the breathing pattern.

Consequences of capsaicin treatment on pulmonary vagal reflexes and chemoreceptor activity in lambs

2000 ◽  
Vol 89 (5) ◽  
pp. 1709-1718 ◽  
Author(s):  
Véronique Diaz ◽  
Julie Arsenault ◽  
Jean-Paul Praud ◽  
Keyword(s):  
Ventilatory Response ◽  
Ventilatory Responses ◽  
Body Activity ◽  
Pulmonary Receptor ◽  
Stretch Receptors ◽  
C Fiber ◽  
Pulmonary Stretch Receptors ◽  
Bolus Intravenous Injection ◽  
To Receive ◽  
Stimulation Of

The aim of this study was to test the hypothesis that capsaicin treatment in lambs selectively inhibits bronchopulmonary C-fiber function but does not alter other vagal pulmonary receptor functions or peripheral and central chemoreceptor functions. Eleven lambs were randomized to receive a subcutaneous injection of either 25 mg/kg capsaicin (6 lambs) or solvent (5 lambs) under general anesthesia. Capsaicin-treated lambs did not demonstrate the classical ventilatory response consistently observed in response to capsaicin bolus intravenous injection in control lambs. Moreover, the ventilatory responses to stimulation of the rapidly adapting pulmonary stretch receptors (intratracheal water instillation) and slowly adapting pulmonary stretch receptors (Hering-Breuer inflation reflex) were similar in both groups of lambs. Finally, the ventilatory responses to various stimuli and depressants of carotid body activity and to central chemoreceptor stimulation (CO2 rebreathing) were identical in control and capsaicin-treated lambs. We conclude that 25 mg/kg capsaicin treatment in lambs selectively inhibits bronchopulmonary C-fiber function without significantly affecting the other vagal pulmonary receptor functions or that of peripheral and central chemoreceptors.

Vasomotor inhibition in rabbits by vagal nonmedullated fibers from cardiopulmonary area

1975 ◽  
Vol 229 (5) ◽  
pp. 1410-1413 ◽  
Author(s):  
PN Thoren ◽  
G Mancia ◽  
JT Shepherd
Keyword(s):  
Blood Pressure ◽  
Vagal Afferents ◽  
Total Contribution ◽  
C Fibers ◽  
Aortic Blood ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Vagal Nerves ◽  
Aortic Blood Pressure ◽  
Aortic Baroreceptors

In anesthetized rabbits with sinus and aortic nerve cut, when the cervical vagal nerves were cooled to 12, 8, 6, and 0degreeC, there were progressive increases in aortic blood pressure of 7 +/- 1, 15 +/- 2, 25 +/- 1, and 41 +/- 2 mmHg (SE), respectively. For comparison, during cooling of the aortic and vagal nerves, at 12degreesC there was a decrease in firing in the afferent fibers from aortic baroreceptors (48 +/- 4%) and pulmonary stretch receptors (57 +/- 5%), and at 6degreesC all activity was abolished. Thus, at 6degreesC the activity in medullated fibers from the aortic baroreceptors and pulmonary stretch receptors is blocked, but the increase in aortic blood pressure with vagal cooling is only 60% of that with cooling to 0degreeC. This demonstrates that cardiopulmonary receptors with nonmedullated vagal afferents (C fibers) contribute to the tonic inhibition of the vasomotor center. Because of overlap in sensitivity of different vagal fibers to cooling, the total contribution of these C fibers cannot be evaluated.

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.

Reflex control of the tracheal vasculature of sheep

1993 ◽  
Vol 75 (5) ◽  
pp. 2173-2179 ◽  
Author(s):  
S. E. Webber ◽  
J. G. Widdicombe
Keyword(s):  
Carotid Body ◽  
Muscle Tone ◽  
Intravenous Injections ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Before And After ◽  
Cervical Trachea ◽  
Carotid Body Chemoreceptors ◽  
Reflex Stimulation ◽  
Stimulation Of

Arteries to the cervical trachea were perfused at constant flow in anesthetized sheep. Perfusion pressures (PP), blood pressure (BP), and changes in tracheal smooth muscle tone (Ptr) were measured. Stimulation of pulmonary C-fiber receptors decreased PP (-6.5%) and BP (-16.8%) and increased Ptr (+61.5%), changes prevented by vagotomy and therefore reflex. Stimulation of cardiac receptors and slowly adapting pulmonary stretch receptors decreased PP (-7.9%) and BP (-21.0) and increased Ptr (+19.0%), changes reversed by vagotomy and therefore reflex. Stimulation and inhibition of slowly adapting pulmonary stretch receptors had no vagal-dependent effect on PP and BP, but inflation decreased (-20.3%) and deflation increased Ptr (+35.2%), effects abolished by vagotomy and therefore reflex. Systemic hypoxia increased PP and BP before and after vagotomy (+12.2 and +40.3%), effects greatly reduced by cutting the carotid body nerves; it increased Ptr (+29.8%), an effect abolished by vagotomy and cutting the carotid body nerves. Systemic hypercapnia increased PP (+16.9%), BP (+20.5%), and Ptr (+36.2%), the first two responses being unaffected by vagotomy and the last almost abolished. Stimulation of carotid body chemoreceptors by KCN increased PP (+22.5%), BP (+104.7%), and Ptr (+8.5%), all responses prevented by cutting the carotid body nerves. Responses to intravenous injections of KCN were similar.

Substance P antagonist does not block the stimulation of rapidly adapting pulmonary stretch receptors by ammonia

Lung ◽  
1994 ◽  
Vol 172 (1) ◽  
Author(s):  
S. Matsumoto ◽  
M. Yamasaki ◽  
T. Kanno ◽  
T. Nagayama ◽  
M. Tanno ◽  
...  
Keyword(s):  
Substance P ◽  
Substance P Antagonist ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Stimulation Of
Sign in / Sign up

Export Citation Format

Share Document