Role of bronchopulmonary C-fiber afferents in the apneic response to cigarette smoke

1987 ◽  
Vol 63 (4) ◽  
pp. 1366-1373 ◽  
Author(s):  
L. Y. Lee ◽  
E. R. Beck ◽  
R. F. Morton ◽  
Y. R. Kou ◽  
D. T. Frazier
Keyword(s):  
Cigarette Smoke ◽  
Control Level ◽  
Vagal Afferents ◽  
Smoke Inhalation ◽  
Coolant Temperature ◽  
Positive Pressure ◽  
Base Line ◽  
Lung Inflation ◽  
C Fiber

The role of vagal bronchopulmonary C-fiber afferents in eliciting the immediate changes in breathing pattern after acute inhalation of cigarette smoke was assessed with a selective blockade of myelinated vagal afferents (innervating both stretch and irritant receptors) utilizing the method of differential cooling. In 15 of 17 chloralose-anesthetized dogs tested, spontaneous inhalation of cigarette smoke (19.7% avg conc, 500–700 ml vol) reproducibly caused the following immediate responses: apnea, bradycardia, and hypotension. These responses occurred within 1 to 2 breaths of smoke inhalation and were followed by a delayed hyperpnea. The apneic duration reached 326 +/- 33% (SE) (n = 15) of the mean base-line expiratory duration. Differential cold block of both vagi (coolant temperature 8.4 +/- 0.3 degrees C) abolished the reflex apnea induced by a positive-pressure (7–10 cmH2O) lung inflation but did not affect the apneic response to smoke inhalation (345 +/- 35%). The smoke-induced apnea was completely abolished by lowering the coolant temperature to -1.3 +/- 0.2 degrees C (n = 10) or by bilateral vagotomy (n = 5) and returned to the control level after both vagi were rewarmed. Based on these results, we suggest that the immediate apneic response to inhaled cigarette smoke is elicited by a stimulation of vagal C-fiber afferents in the lungs and airways.

Reflex control of breathing following inhalation of cigarette smoke in conscious dogs

1983 ◽  
Vol 54 (2) ◽  
pp. 562-570 ◽  
Author(s):  
L. Y. Lee ◽  
R. F. Morton ◽  
A. H. Hord ◽  
D. T. Frazier
Keyword(s):  
Cigarette Smoke ◽  
Carotid Body ◽  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Vagal Afferents ◽  
Smoke Inhalation ◽  
Base Line ◽  
Mean Values ◽  
Carotid Body Chemoreceptors

The acute ventilatory response to spontaneously inhaled cigarette smoke (750 ml, 10% concentration) was studied in 92 experiments on 6 awake resting dogs. Upon the first or second breath of smoke inhalation, either an apnea or an augmented breath was elicited consistently in each dog, and a hyperpnea occurred subsequently. Minute ventilation (VE) increased from a base line of 3.2 to a peak of 23.9 l/min at 8.3 s (mean values) after the smoke was completely inhaled and returned toward base line in 1–3 min. Cold blocking of both vagi (exteriorized in skin loops) eliminated the initial change in breathing pattern but did not significantly reduce the delayed hyperpnea. Denervation of carotid body chemoreceptors alone abolished 71.5% of the increase in VE induced by cigarette smoke. These results suggest that the apnea or augmented breath immediately following the smoke inhalation is mediated through vagal afferents, whereas the delayed hyperpnea results primarily from the stimulation of carotid body chemoreceptors, presumably by the absorbed nicotine.

Acute effects of cigarette smoke on breathing in rats: vagal and nonvagal mechanisms

1990 ◽  
Vol 68 (3) ◽  
pp. 955-961 ◽  
Author(s):  
L. Y. Lee ◽  
R. F. Morton ◽  
Y. R. Kou
Keyword(s):  
Cigarette Smoke ◽  
Initial Response ◽  
Inhibitory Effect ◽  
Smoke Inhalation ◽  
Delayed Response ◽  
Base Line ◽  
Sprague Dawley ◽  
Lung Inflation ◽  
Shallow Breathing ◽  
Bilateral Vagotomy

The acute ventilatory response to inhalation of cigarette smoke was studied in anesthetized Sprague-Dawley rats. Cigarette smoke (6 ml, 50%) generated by a machine was inhaled spontaneously via a tracheal cannula. Within the first two breaths of smoke inhalation, a slowing of respiration resulting from a prolonged expiratory duration (173 +/- 6% of the base line; n = 32) was elicited in 88% of the rats studied. This initial inhibitory effect on breathing was not affected either by an increase (410%) in the nicotine content of the cigarette smoke or by pretreatment with hexamethonium (33 mg/kg iv). However, bilateral vagotomy completely eliminated the initial ventilatory inhibition. Cooling both vagi to 5.1 degrees C blocked the reflex apneic response to lung inflation, but it did not abolish the inhibitory effect of smoke. After the initial response, a rapid shallow breathing pattern developed and reached its peak 5-12 breaths after inhalation of high-nicotine cigarette smoke; this delayed response could not be prevented by vagotomy and was undetectable after inhalation of low-nicotine smoke. We conclude that the initial inhibitory effect of smoke on breathing is mediated by vagal bronchopulmonary C-fiber afferents, which are stimulated by smoke constituents other than nicotine, whereas the delayed tachypneic response to smoke is caused by the absorbed nicotine.

Acute effect of cigarette smoke on cytoplasmic motility of alveolar macrophages in dogs

1989 ◽  
Vol 66 (3) ◽  
pp. 1172-1178 ◽  
Author(s):  
M. Yamaya ◽  
K. Zayasu ◽  
K. Sekizawa ◽  
K. Yamauchi ◽  
S. Shimura ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Alveolar Macrophages ◽  
Lower Lobe ◽  
The Body ◽  
Sensory Nerves ◽  
Smoke Inhalation ◽  
Base Line ◽  
Particle Rotation ◽  
Lobe Bronchus

To study effects of cigarette smoke on the cytoplasmic motility (CM) of alveolar macrophages (AM), we measured remanent field strength (RFS) in dogs in vivo. Four days after instillation of ferrimagnetic particles (Fe3O4, 3 mg/kg) into the right lower lobe bronchus, RFS was measured at the body surface immediately after magnetization of the Fe3O4 particles by an externally applied magnetic field. RFS decreased with time due to particle rotation (relaxation), which is thought to be inversely related to CM of AM (J. Appl. Physiol. 55: 1196–1202, 1983). The initial relaxation curve was fitted to an exponential function. The relaxation rate (lambda 0) increased during cigarette smoke inhalation and returned to base-line values within 15 min. With the inhalation of the smoke of up to five cigarettes, peak lambda 0 was increased; with a further increase in the number of cigarettes, the effect of cigarette smoke decreased or disappeared. Nicotine injection and acetylcholine inhalation increased respiratory resistance to a degree similar to that observed with cigarette smoke but did not change lambda 0. However, either substance P (SP) or capsaicin injection increased lambda 0 in a fashion similar to that noted with cigarette smoke inhalation. Repeated administration of SP produced a significant tachyphylaxis of the effect, and capsaicin did not increase lambda 0 after the cigarette smoke-induced tachyphylaxis of the effect. Colchicine inhibited the cigarette smoke-induced increase in lambda 0. These results suggest that cigarette smoke increases CM of AM, probably through the release of tachykinins including SP from sensory nerves in the lung.

Alveolar hypercapnia augments pulmonary C-fiber responses to chemical stimulants: role of hydrogen ion

2002 ◽  
Vol 93 (1) ◽  
pp. 181-188 ◽  
Author(s):  
Qihai Gu ◽  
Lu-Yuan Lee
Keyword(s):  
Hydrogen Ion ◽  
Right Atrial ◽  
Mechanical Stimuli ◽  
Hydrogen Ions ◽  
Lung Inflation ◽  
C Fibers ◽  
Arterial Blood ◽  
Blood Ph ◽  
C Fiber

To determine whether the excitabilities of pulmonary C fibers to chemical and mechanical stimuli are altered by CO2-induced acidosis, single-unit pulmonary C-fiber activity was recorded in anesthetized, open-chest rats. Transient alveolar hypercapnia (HPC) was induced by administering CO2-enriched gas mixture (15% CO2, balance air) via the respirator inlet for 30 s, which rapidly lowered the arterial blood pH from a baseline of 7.40 ± 0.01 to 7.17 ± 0.02. Alveolar HPC markedly increased the responses of these C-fiber afferents to several chemical stimulants. For example, the C-fiber response to right atrial injection of the same dose of capsaicin (0.25–1.0 μg/kg) was significantly increased from 3.07 ± 0.70 impulses/s at control to 8.48 ± 1.52 impulses/s during HPC ( n = 27; P < 0.05), and this enhanced response returned to control within ∼10 min after termination of HPC. Similarly, alveolar HPC also induced significant increases in the C-fiber responses to right atrial injections of phenylbiguanide (4–8 μg/kg) and adenosine (0.2 mg/kg). In contrast, HPC did not change the response of pulmonary C fibers to lung inflation. Furthermore, the peak response of these C fibers to capsaicin during HPC was greatly attenuated when the HPC-induced acidosis was buffered by infusion of bicarbonate (1.36–1.82 mmol · kg−1 · min−1 for 35 s). In conclusion, alveolar HPC augments the responses of these afferents to various chemical stimulants, and this potentiating effect of CO2 is mediated through the action of hydrogen ions on the C-fiber sensory terminals.

Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs

1997 ◽  
Vol 83 (3) ◽  
pp. 958-965 ◽  
Author(s):  
Zhong-Xin Wu ◽  
Robert F. Morton ◽  
Lu-Yuan Lee
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Lung Compliance ◽  
Smoke Inhalation ◽  
Before And After ◽  
Sham Exposure ◽  
Inhalation Challenge ◽  
Dynamic Lung Compliance

Wu, Zhong-Xin, Robert F. Morton, and Lu-Yuan Lee. Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs. J. Appl. Physiol. 83(3): 958–965, 1997.—Acute exposure to ozone (O3) induces airway hyperresponsiveness to various inhaled bronchoactive substances. Inhalation of cigarette smoke, a common inhaled irritant in humans, is known to evoke a transient bronchoconstrictive effect. To examine whether O3 increases airway responsiveness to cigarette smoke, effects of smoke inhalation challenge on total pulmonary resistance (Rl) and dynamic lung compliance (Cdyn) were compared before and after exposure to O3 (1.5 ppm, 1 h) in anesthetized guinea pigs. Before O3 exposure, inhalation of two breaths of cigarette smoke (7 ml) at a low concentration (33%) induced a mild and reproducible bronchoconstriction that slowly developed and reached its peak (ΔRl= 67 ± 19%, ΔCdyn = −29 ± 6%) after a delay of >1 min. After exposure to O3 the same cigarette smoke inhalation challenge evoked an intense bronchoconstriction that occurred more rapidly, reaching its peak (ΔRl = 620 ± 224%, ΔCdyn = −35 ± 7%) within 20 s, and was sustained for >2 min. By contrast, sham exposure to room air did not alter the bronchomotor response to cigarette smoke challenge. Pretreatment with CP-99994 and SR-48968, the selective antagonists of neurokinin type 1 and 2 receptors, respectively, completely blocked the enhanced responses of Rl and Cdyn to cigarette smoke challenge induced by O3. These results show that O3 exposure induces airway hyperresponsiveness to inhaled cigarette smoke and that the enhanced responses result primarily from the bronchoconstrictive effect of endogenous tachykinins.

scholarly journals Hypertonic saline stimulates vagal afferents that respond to lung deflation

2019 ◽  
Vol 317 (6) ◽  
pp. R814-R817
Author(s):  
Juan Guardiola ◽  
Mohamed Saad ◽  
Jerry Yu
Keyword(s):  
Hypertonic Saline ◽  
Single Unit ◽  
Direct Injection ◽  
Control Level ◽  
Receptive Fields ◽  
Vagal Afferents ◽  
Lung Inflation ◽  
Mechanically Ventilated ◽  
Lung Deflation ◽  
Increased Activity

In our present studies, we seek to determine whether increased osmolarity stimulates deflation-activated receptors (DARs). In anesthetized, open-chest, and mechanically ventilated rabbits, we recorded single-unit activities from typical slowly adapting receptors (SARs; responding only to lung inflation) and DAR-containing SARs (DAR-SARs; responding to both lung inflation and deflation) and identified their receptive fields in the lung. We examined responses of these two groups of pulmonary sensory units to direct injection of hypertonic saline (8.1% sodium chloride; 9-fold in tonicity) into the receptive fields. Hypertonic saline decreased the activity in most SAR units from 40.3 ± 5.4 to 34.8 ± 4.7 imp/s ( P < 0.05, n = 12). In contrast, it increased the activity in DAR-SAR units quickly and significantly from 15.9 ± 2.2 to 43.4 ± 10.0 imp/s ( P < 0.01, n = 10). Many units initially had increased activity, mainly in the deflation phase. DAR-SAR activities largely returned to the control level 30 s after injection. Since hypertonic saline stimulated DAR-SAR units but not SAR units, we conclude that hypertonic saline activates DARs.

Selected Contribution: Hypersensitivity of pulmonary C fibers induced by adenosine in anesthetized rats

2003 ◽  
Vol 95 (3) ◽  
pp. 1315-1324 ◽  
Author(s):  
Qihai Gu ◽  
Ting Ruan ◽  
Ju-Lun Hong ◽  
Nausherwan Burki ◽  
Lu-Yuan Lee
Keyword(s):  
Receptor Antagonist ◽  
Potential Role ◽  
Right Atrial ◽  
Adenosine Infusion ◽  
Lung Inflation ◽  
C Fibers ◽  
Baseline Activity ◽  
Tracheal Pressure ◽  
C Fiber

Compelling clinical evidence implicates the potential role of adenosine in development of airway hyperresponsiveness and suggests involvement of pulmonary sensory receptors. This study was carried out to determine the effect of a low dose of adenosine infusion on sensitivity of pulmonary C-fiber afferents in anesthetized open-chest rats. Infusion of adenosine (40 μg · kg-1 · min-1 iv for 90 s) mildly elevated baseline activity of pulmonary C fibers. However, during adenosine infusion, pulmonary C-fiber responses to chemical stimulants and lung inflation (30 cmH2O tracheal pressure) were markedly potentiated; e.g., the response to right atrial injection of capsaicin (0.25 or 0.5 μg/kg) was increased by more than fivefold (change in fiber activity = 2.64 ± 0.67 and 16.27 ± 3.11 impulses/s at control and during adenosine infusion, n = 13, P < 0.05), and this enhanced response returned to control in ∼10 min. The potentiating effect of adenosine infusion was completely blocked by pretreatment with 8-cyclopentyl-1,3-dipropylxanthine (100 μg/kg), a selective antagonist of the adenosine A1 receptor, but was not affected by 3,7-dimethyl-1-propargylxanthine (1 mg/kg), an A2-receptor antagonist, or 3-ethyl-5-benzyl-2-methyl-4-phenylethynyl-6-phenyl-1,4-(±)-dihydropyridine-3,5-dicarboxylate (2 mg/kg), an A3-receptor antagonist. This potentiating effect was also mimicked by N6-cyclopentyladenosine (0.25 μg·kg-1·min-1 for 90 s), a selective agonist of the adenosine A1 receptor. In conclusion, our results showed that infusion of adenosine significantly elevated the sensitivity of pulmonary C-fiber afferents in rat lungs and that this potentiating effect is likely mediated through activation of the adenosine A1 receptor.

Acute effects of acrolein on breathing: role of vagal bronchopulmonary afferents

1992 ◽  
Vol 72 (3) ◽  
pp. 1050-1056 ◽  
Author(s):  
B. P. Lee ◽  
R. F. Morton ◽  
L. Y. Lee
Keyword(s):  
Inhibitory Effect ◽  
Acute Effects ◽  
Afferent Stimulation ◽  
Lung Inflation ◽  
Anesthetized Rats ◽  
C Fiber ◽  
Bilateral Vagotomy ◽  
Irritant Receptors

Spontaneous inhalation of acrolein vapor (350 ppm, 1 ml/100 g body wt) elicited an immediate and transient inhibitory effect on breathing in anesthetized rats, characterized by a prolongation of expiratory duration and accompanied by a bradycardia; ventilation was reduced by 47 +/- 6%, which returned to baseline after three to seven breaths. When both vagi were cooled to 6.6 +/- 0.1 degrees C, the reflex apneic response to lung inflation was completely abolished but the bradypneic response to acrolein was not affected. After perineural capsaicin treatment of both cervical vagi to selectively block the capsaicin-sensitive C-fiber afferents, acrolein no longer evoked an inhibitory effect on breathing; conversely, an augmented inspiration was consistently elicited with the first breath of acrolein inhalation, which was subsequently abolished by cooling both vagi to 6.5 degrees C. The inhibitory effect of inhaling acrolein at a lower concentration (200 ppm) was not detectable, whereas that of a higher concentration (600 ppm) was more intense and prolonged. All these responses were completely eliminated by bilateral vagotomy. These results suggest that inhaled acrolein activated both vagal C-fiber endings and rapidly adapting irritant receptors in the airways, but the acrolein-induced inhibitory effect on breathing was elicited primarily by the C-fiber afferent stimulation.

Evidence for cardiac volume-receptor regulation of feline jejunal blood flow and fluid transport

1984 ◽  
Vol 246 (4) ◽  
pp. G401-G410 ◽  
Author(s):  
H. Sjovall ◽  
S. Redfors ◽  
B. Biber ◽  
J. Martner ◽  
O. Winso
Keyword(s):  
Blood Flow ◽  
Fluid Transport ◽  
Positive Pressure Ventilation ◽  
Intestinal Secretion ◽  
Vagal Afferents ◽  
Positive Pressure ◽  
Cardiac Volume ◽  
Jejunal Segment ◽  
Inspiratory Resistance

The aim of the study was to investigate the role of cardiac mechanoreceptors in the reflex regulation of intestinal blood flow and fluid transport. Feline cardiac mechanoreceptor activity was modified with two noninvasive techniques: positive-pressure ventilation (PPV) and inspiratory resistance breathing (IRB). A jejunal segment with intact vascular and nervous supply was isolated and exposed to cholera toxin as a model for intestinal secretion. The results revealed that PPV induced a pronounced intestinal vasoconstriction and a marked inhibition of choleraic secretion. IRB had the opposite effects. The responses were well correlated with changes in central blood volume and either markedly reduced or abolished by vagotomy, intestinal alpha-adrenoreceptor blockade, or postganglionic mesenteric denervation. The results indicate that cardiac mechanoreceptors with vagal afferents may mediate the observed reflex responses, and hence this receptor station may be of importance in the normal reflex control of intestinal hemodynamics and fluid transport.

scholarly journals Role of vagal fibers in the hypoxia-induced increases in end-expiratory lung volume and diaphragmatic activity

1997 ◽  
Vol 83 (3) ◽  
pp. 700-706 ◽  
Author(s):  
M. Bonora ◽  
M. Vizek
Keyword(s):  
Lung Volume ◽  
Breathing Pattern ◽  
Vagal Afferents ◽  
C Fibers ◽  
C Fiber ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Ventilatory Response To Hypoxia ◽  
Intact Rats

Bonora, M., and M. Vizek. Role of vagal fibers in the hypoxia-induced increases in end-expiratory lung volume and diaphragmatic activity. J. Appl. Physiol. 83(3): 700–706, 1997.—The possible role of pulmonary C fibers in the hypoxia-induced concomitant increases in end-expiratory lung volume (EELV) and in the activity of the diaphragm at the end of expiration (De) were evaluated by measuring the effects of hypoxia (10% O2) on ventilation, EELV, and De in eight chloralose-urethan anesthetized rats. Recordings were made before and after blocking vagal C fibers and after bilateral vagotomy. C-fiber conduction was blocked by applying capsaicin perineurally to the cervical vagi. The efficiency of C-fiber blockade was tested with intravenous capsaicin and its selectivity by the Hering-Breuer reflex. Perineural capsaicin abolished the reflex apnea induced by intravenous capsaicin and transiently reduced Hering-Breuer reflex. Perineural capsaicin affected neither ventilation, De, and EELV in air nor the hypoxia-induced increases in these parameters. Vagotomy caused the typical changes of breathing pattern in air, but the ventilatory response to hypoxia was unchanged. Vagotomy performed during hypoxia resulted in large decreases in De and EELV. Hypoxia increased De and EELV in vagotomized rats but less than in intact rats. We conclude that the hypoxia-induced increases in EELV and diaphragmatic activity are probably not mediated by vagal C fibers and that vagal afferents are involved but not fully responsible for this phenomenon.

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