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.

Diaphragmatic responses to graded stimulation of pulmonary C-fibers with capsaicin

1985 ◽  
Vol 59 (5) ◽  
pp. 1487-1494 ◽  
Author(s):  
J. R. Coast ◽  
S. S. Cassidy
Keyword(s):  
Dose Response ◽  
Strain Gauge ◽  
Contraction Rate ◽  
C Fibers ◽  
C Fiber ◽  
Shallow Breathing ◽  
Fiber Stimulation ◽  
Rapid Shallow Breathing ◽  
Stimulation Of

It has been suggested that pulmonary C-fiber stimulation is responsible for the rapid shallow breathing that accompanies pulmonary edema. However, pulmonary C-fiber stimulation also causes apnea. To determine whether it was possible for both responses to occur from one stimulus, we infused varying concentrations of capsaicin (a compound that selectively stimulates C-fiber receptors in the dog) into an in situ vascularly isolated dog lung and measured rates and strengths of diaphragmatic contractions with a strain gauge sutured to the diaphragm and electromyogram electrodes implanted in the diaphragm. There was a dose response to capsaicin in that increased doses were related directly with the duration of cessation of diaphragmatic contractions (2–100 s) and inversely with the latency from the start of stimulation to the beginning of the cessation of diaphragmatic contractions (100–5 s). There was no evidence, however, of rapid shallow breathing in this set of experiments. Either a gradual return to normal rate from prolonged contraction intervals or no change in contraction rate was seen, depending on capsaicin concentration. We conclude that the primary diaphragmatic response to pulmonary C-fiber stimulation is a cessation of diaphragmatic contractions rather than rapid shallow contractions.

Rapid shallow breathing evoked by capsaicin from isolated pulmonary circulation

1986 ◽  
Vol 61 (3) ◽  
pp. 1237-1240 ◽  
Author(s):  
E. R. Schertel ◽  
L. Adams ◽  
D. A. Schneider ◽  
K. S. Smith ◽  
J. F. Green
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Circulation ◽  
Nerve Activity ◽  
C Fibers ◽  
Shallow Breathing ◽  
Pulmonary Arterial ◽  
Alpha Chloralose ◽  
Spontaneously Breathing ◽  
Rapid Shallow Breathing ◽  
Stimulation Of

Recently Green et al. (J. Appl. Physiol. 57:562–567, 1984) reported that pulmonary C-fibers initiate the prompt apnea evoked by pulmonary arterial injections of capsaicin; however, their role in the subsequent rapid shallow breathing of the pulmonary chemoreflex is still in dispute. To determine whether this reflex tachypnea is triggered by pulmonary C-fibers rather than by afferents further downstream, we separately perfused the pulmonary and systemic circulations in dogs anesthetized with either halothane or alpha-chloralose as the lungs were ventilated with a servo-controlled ventilator driven by phrenic nerve activity. Injection of capsaicin (10 micrograms/kg) into the pulmonary artery of the isolated pulmonary circulation evoked an immediate apnea followed by rapid shallow breathing. Injection of the same dose of capsaicin into the left atrium of the isolated pulmonary circulation had no effect. By contrast, when capsaicin was administered at a slower rate into the pulmonary artery (10–20 micrograms X kg-1 X min-1) rapid shallow breathing occurred but without apnea. Our results are consistent with the hypothesis that in spontaneously breathing animals, stimulation of pulmonary C-fibers can evoke rapid shallow breathing.

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 C-fibers evoke both apnea and tachypnea of pulmonary chemoreflex

1984 ◽  
Vol 57 (2) ◽  
pp. 562-567 ◽  
Author(s):  
J. F. Green ◽  
N. D. Schmidt ◽  
H. D. Schultz ◽  
A. M. Roberts ◽  
H. M. Coleridge ◽  
...  
Keyword(s):  
Transpulmonary Pressure ◽  
Systemic Circulation ◽  
Burst Frequency ◽  
C Fibers ◽  
Shallow Breathing ◽  
Anesthetized Dogs ◽  
Pulmonary Arterial ◽  
Spontaneously Breathing ◽  
Rapid Shallow Breathing ◽  
Stimulation Of

Pulmonary C-fibers initiate the prompt apnea evoked by pulmonary arterial injections of capsaicin, but their role in the subsequent rapid shallow breathing of the pulmonary chemoreflex is disputed. To determine whether this reflex tachypnea is triggered by pulmonary C-fibers rather than by afferents further downstream, we separately perfused the pulmonary and systemic circulation in anesthetized dogs. When the lungs were rhythmically inflated, injection of capsaicin (0.5–20.0 micrograms X kg-1) into the isolated pulmonary circulation evoked an immediate cessation of phrenic nerve firing (“apnea”) and when phrenic bursts resumed, a reduction in their amplitude. Phrenic burst frequency was usually entrained to the ventilator cycle and did not increase. By contrast, when entrainment of phrenic bursts was avoided by statically inflating the lungs at a transpulmonary pressure of 3 cmH2O, the injection of capsaicin evoked apnea, followed by a prolonged increase in phrenic burst frequency and a decrease in amplitude (“rapid shallow breathing”). The infusion of capsaicin (10–20 micrograms X kg-1 X min-1) also evoked rapid shallow breathing, but without apnea. Our results are consistent with the hypothesis that in spontaneously breathing animals, stimulation of pulmonary C-fibers evokes rapid shallow breathing.

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.

Effect of changing body temperature on the ventilatory and metabolic responses of lean and obese Zucker rats

1998 ◽  
Vol 275 (2) ◽  
pp. R531-R540 ◽  
Author(s):  
Michael Maskrey ◽  
David Megirian ◽  
Gaspar A. Farkas
Keyword(s):  
Body Temperature ◽  
Breathing Pattern ◽  
Ventilation Rate ◽  
Zucker Rats ◽  
Obese Rats ◽  
Shallow Breathing ◽  
Obese Zucker Rats ◽  
Metabolic Variables ◽  
The Difference ◽  
Rapid Shallow Breathing

We measured body temperature (Tb) and ventilatory and metabolic variables in lean ( n = 8) and obese ( n = 8) Zucker rats. Measurements were made while rats breathed air, 4% CO2, and 10% O2. Under control conditions, Tb in obese rats was always less than that of their lean counterparts. Obese rats adopted a more rapid, shallow breathing pattern than lean rats in air and had a lower ventilation rate in 4% CO2. Respiration in 10% O2 was similar for the two groups. Metabolic variables did not differ between lean and obese rats whatever the gas breathed. When lean rats were cooled to match Tb in control obese rats with an implanted abdominal heat exchanger, they increased ventilation and metabolism in air; there was no effect of cooling on responses to 4% CO2; and ventilation increased while metabolism decreased in 10% O2. When obese rats were warmed to match Tb in control lean rats, trends in ventilation and metabolism resulted in a tendency toward hyperventilation in air and 4% CO2, but not in 10% O2. Taken overall, matching Tb in lean and obese rats accentuated differences in respiratory and metabolic variables between the two groups. We conclude that differences in respiration between lean and obese Zucker rats are not due to the difference in Tb.

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.

Airway responses to histamine and methocholine in Ascaris suum-allergic rhesus monkeys

1978 ◽  
Vol 45 (6) ◽  
pp. 846-851 ◽  
Author(s):  
M. C. Michoud ◽  
P. D. Pare ◽  
R. Boucher ◽  
J. C. Hogg
Keyword(s):  
Rhesus Monkeys ◽  
Breathing Pattern ◽  
Ascaris Suum ◽  
Pulmonary Resistance ◽  
Response Curves ◽  
Equal Degree ◽  
Wide Range ◽  
Shallow Breathing ◽  
Airway Responses ◽  
Rapid Shallow Breathing

We performed dose-response curves to inhaled histamine (H) and methacholine (MC) in a group of eight rhesus monkeys, with and without natural allergy to Ascaris suum antigen (AA). The animals were anesthetized with pentobarbital sodium, 25 mg/kg im and studied in a volume-displacement body plethysmograph. The dose of H or MC producing a 50% increase in pulmonary resistance (RL) was used to determine sensitivity to these agents and the increase in RL at a given dose was employed as a measure of reactivity. Sensitivity and reactivity to H and MC were then compared with AA responsiveness. A wide range of responses was observed but allergic animals were not more sensitive or reactive to H or MC than nonallergic animals. In addition, we studied the changes in breathing pattern that occurred during the inhalation of AA, H, and MC in four AA-sensitive animals. AA and H produced rapid shallow breathing within 30 s of starting inhalation, but MC, despite causing an equal degree of bronchoconstriction, did not produce alterations in breathing pattern.

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