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.

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.

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.

The involvement of hydroxyl radical and cyclooxygenase metabolites in the activation of lung vagal sensory receptors by circulatory endotoxin in rats

2005 ◽  
Vol 98 (2) ◽  
pp. 620-628 ◽  
Author(s):  
Ching Jung Lai ◽  
Ting Ruan ◽  
Yu Ru Kou
Keyword(s):  
Hydroxyl Radical ◽  
Hydroxyl Radicals ◽  
Lung Compliance ◽  
Radical Scavenger ◽  
C Fibers ◽  
C Fiber ◽  
Underlying Mechanisms ◽  
Dynamic Lung Compliance ◽  
Fiber Stimulation ◽  
Stimulation Of

Circulatory endotoxin can stimulate vagal pulmonary C fibers and rapidly adapting receptors (RARs) in rats, but the underlying mechanisms are not clear. We investigated the involvement of hydroxyl radicals and cyclooxygenase metabolites in the stimulation of C fibers and RARs by circulatory endotoxin (50 mg/kg) in 112 anesthetized, paralyzed, and artificially ventilated rats. In rats pretreated with the vehicle, endotoxin stimulated C fibers and RARs and caused a slight increase in total lung resistance (Rl) and a decrease in dynamic lung compliance. In rats pretreated with dimethylthiourea (a hydroxyl radical scavenger) alone, indomethacin (a cyclooxygenase inhibitor) alone, or a combination of the two, C-fiber and RAR responses [C fiber: change (Δ) = −62, −79, and −85%; RAR: Δ = −80, −84, and −84%, respectively] were reduced, and the Rl response was prevented. The suppressive effects of a combination of dimethylthiourea and indomethacin on the C-fiber and RAR responses were not superior to indomethacin alone. In rats pretreated with isoproterenol (a bronchodilator), the C-fiber response was not significantly affected (Δ = −26%), the RAR response was reduced (Δ = −88%), and the Rl response was prevented. None of these pretreatments affected the dynamic lung compliance response. These results suggest that 1) both hydroxyl radicals and cyclooxygenase metabolites are involved in the endotoxin-induced stimulation of C fibers and RARs, and 2) the involvement of these two metabolites in the C-fiber stimulation may be due to their chemical effects, whereas that in the RAR stimulation may be due to their bronchoconstrictive effects.

Lung dysfunction after thermal injury in relation to prostanoid and oxygen radical release

1986 ◽  
Vol 61 (1) ◽  
pp. 103-112 ◽  
Author(s):  
L. J. Jin ◽  
C. Lalonde ◽  
R. H. Demling
Keyword(s):  
Lipid Peroxidation ◽  
Lung Tissue ◽  
Lipid Peroxide ◽  
Lung Compliance ◽  
Base Line ◽  
Lung Water ◽  
Control Value ◽  
Lung Dysfunction ◽  
Dynamic Lung Compliance ◽  
Lung Lymph

We studied whether changes in lung function after burns (1- to 12-h period) were due to changes in lung water or airways resistance and the relationship of the changes to prostanoid and O2 radical activity (measured as lipid peroxidation). Twenty-five anesthetized mechanically ventilated adult sheep were given a 40% of body surface scald burn and resuscitated to restore and maintain base-line filling pressures. Dynamic lung compliance (Cdyn) decreased by 40% from 38 +/- 5 to 24 +/- 4 ml/cmH2O at 12 h. Venous thromboxane B2 transiently increased from 210 +/- 40 to 1,100 +/- 210 pg/ml, and the value in lung lymph increased from 180 +/- 80 to 520 +/- 80 pg/ml. Prostacyclin levels in lung lymph and plasma remained at base line. Protein-poor lung lymph flow increased two- to threefold, but postmortem lung analysis revealed no increase in lung water from the control of 3.5 +/- 0.3 g H2O/g dry wt. No increase in protein permeability was seen. However, the lipid peroxidation of lung tissue measured as malondialdehyde was significantly increased from the control value of 56 +/- 4 nmol/g lung to a value of 69 +/- 6. Ibuprofen pretreatment (12.5 mg/kg) markedly attenuated the decrease in Cdyn, with the value at 12 h being 90% of base line. Ibuprofen also decreased the amount of lung lipid peroxidation but did not decrease the lung lymph response. We conclude that the decrease in Cdyn seen early postburn is not due to increased lung water, but, rather, is due to a mediator-induced bronchoconstriction, attenuated by ibuprofen; the mediator being either thromboxane or a byproduct of O2 radicals as evidenced by increased lipid peroxide production in lung tissue.

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs

1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  
Keyword(s):  
Gland Secretion ◽  
Right Atrial ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Submucosal Glands ◽  
C Fiber ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

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.

Acute effects of atrial natriuretic peptide on lung mechanics and hemodynamics in awake sheep

1990 ◽  
Vol 69 (2) ◽  
pp. 728-733 ◽  
Author(s):  
M. R. Banerjee ◽  
J. H. Newman
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pulmonary Arteries ◽  
Lung Compliance ◽  
Lung Mechanics ◽  
Base Line ◽  
Hemodynamic Effects ◽  
Airway Response ◽  
Dynamic Lung Compliance ◽  
Atrial Natriuretic

The purpose of this study was to measure airway and hemodynamic effects of atrial natriuretic peptide (ANP) and its efficacy in counteracting the changes in lung mechanics that occur with aerosol histamine and carbachol. Synthetic human alpha-ANP was injected into the pulmonary arteries of awake sheep chronically instrumented for measurement of lung mechanics and hemodynamics (n = 7). Base-line dynamic lung compliance (Cdyn) and pulmonary resistance (RL) did not change after ANP injection. On separate days, the dose required to reduce Cdyn to 65% of base line (ED65Cdyn) to progressive doses of aerosol histamine and the dose required to increase RL by 100% of the base-line values (ED200RL) to progressive doses of aerosol carbachol were determined. ANP was given as bolus injections of 1, 5, and 10 micrograms/kg 3 min after either the ED65Cdyn or ED200RL doses of histamine and carbachol, respectively, and the airway response was monitored for 10 min. ANP significantly reversed the rise in RL after carbachol administration (n = 10). This action of ANP was not altered by cyclooxygenase inhibition with ibuprofen. ANP did not reverse the reduction in Cdyn caused by either histamine (n = 7) or carbachol. The bronchodilating effect of ANP appears to be more prominent in the larger central airways than in the peripheral airways. The hemodynamic effects of ANP were similar to those reported by others. Heart rate and cardiac output had a biphasic response, with an initial rise followed by a drop below the base line. Systemic arterial and left atrial pressures decreased significantly. Pulmonary arterial pressure did not change significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Pulmonary mechanics during the ventilatory response to hypoxemia in the newborn monkey

1983 ◽  
Vol 55 (3) ◽  
pp. 1008-1014 ◽  
Author(s):  
W. A. LaFramboise ◽  
R. D. Guthrie ◽  
T. A. Standaert ◽  
D. E. Woodrum
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Lung Compliance ◽  
Pulmonary Mechanics ◽  
Base Line ◽  
Respiratory Drive ◽  
Pulmonary Resistance ◽  
Residual Capacity ◽  
Dynamic Lung Compliance ◽  
Sustained Increase

Dynamic lung compliance (CL), inspiratory pulmonary resistance (RL), and functional residual capacity (FRC) were measured in 10 unanesthetized 48 h-old newborn monkeys and seven 21-day-old infant monkeys during acute exposures to an equivalent level of hypoxemia. End-expiratory airway occlusions were performed and the pressure developed by 200 ms (P0.2) was utilized as an index of central respiratory drive. P0.2 demonstrated a sustained increase throughout the period of hypoxemia on day 2 despite the fact that minute ventilation (VI) initially increased but then fell back to base-line levels. Dynamic lung compliance fell and FRC increased by 5 min of hypoxemia in the newborns. The 21-day-old monkeys exhibited a sustained increase in both VI and P0.2 throughout the hypoxic period with no change in CL and FRC. RL did not change at either postnatal age during hypoxemia. These data indicate that the neonatal monkey is subject to changes in pulmonary mechanics (decreased CL and increased FRC) during hypoxemia and that these changes are eliminated with maturation.

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

2003 ◽  
Vol 94 (5) ◽  
pp. 1987-1998 ◽  
Author(s):  
Ting Ruan ◽  
Ching-Yin Ho ◽  
Yu Ru Kou
Keyword(s):  
Initial Response ◽  
Oxygen Species ◽  
C Fibers ◽  
Anesthetized Rats ◽  
Afferent Vagal ◽  
Vagal Cooling ◽  
Saline Vehicle ◽  
Respiratory Reflexes ◽  
Stimulation Of ◽  
Do So

We investigated the afferent vagal pathways mediating respiratory reflexes evoked by reactive oxygen species (ROS) in the lungs of anesthetized rats. Spontaneous inhalation of 0.2% aerosolized H2O2 acutely evoked initial bradypnea followed by delayed tachypnea, which was frequently mixed with delayed augmented inspiration. The initial response was abolished after perivagal capsaicin treatment (PCT), but was prolonged during vagal cooling (VC) to 7°C; PCT and VC are known to differentially block the conduction of unmyelinated C and myelinated fibers, respectively. The delayed responses were eliminated during VC but emerged earlier after PCT. Vagotomy, catalase (an antioxidant for H2O2), dimethylthiourea (an antioxidant for · OH), or deferoxamine (an antioxidant for · OH) largely or totally suppressed these reflexive responses, whereas sham nerve treatment, heat-inactivated catalase, saline vehicle, or iron-saturated deferoxamine failed to do so. These results suggest that 1) the H2O2-evoked initial and delayed airway reflexes are antagonistic and may result from stimulation of lung C fibers and rapidly adapting receptors, respectively, and 2) the reflex effects of H2O2 are, in part, due to the action of · OH on these afferents.

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