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.

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation

1975 ◽  
Vol 39 (3) ◽  
pp. 411-416 ◽  
Author(s):  
D. Heistad ◽  
F. M. Abboud ◽  
A. L. Mark ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Ventilatory Response ◽  
Carotid Bifurcation ◽  
Carotid Chemoreceptors ◽  
Ventilatory Responses ◽  
Before And After ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Baroreceptor Activation ◽  
Stimulation Of

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

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.

Modulation of upper airway muscle activities by bronchopulmonary afferents

2006 ◽  
Vol 101 (2) ◽  
pp. 609-617 ◽  
Author(s):  
E. Fiona Bailey ◽  
Ralph F. Fregosi
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Review Of The Literature ◽  
Lung Inflation ◽  
Hyoid Arch ◽  
Lack Of Information ◽  
Stretch Receptors ◽  
C Fiber ◽  
Pulmonary Stretch Receptors ◽  
Upper Airway Muscles

Here we review the influence of bronchopulmonary receptors (slowly and rapidly adapting pulmonary stretch receptors, and pulmonary/bronchial C-fiber receptors) on respiratory-related motor output to upper airway muscles acting on the larynx, tongue, and hyoid arch. Review of the literature shows that all muscles in all three regions are profoundly inhibited by lung inflation, which excites slowly adapting pulmonary stretch receptors. This widespread coactivation includes the recruitment of muscles that have opposing mechanical actions, suggesting that the stiffness of upper airway muscles is highly regulated. A profound lack of information on the modulation of upper airway muscles by rapidly adapting receptors and bronchopulmonary C-fiber receptors prohibits formulation of a conclusive opinion as to their actions and underscores an urgent need for new studies in this area. The preponderance of the data support the view that discharge arising in slowly adapting pulmonary stretch receptors plays an important role in the initiation of the widespread and highly coordinated recruitment of laryngeal, tongue, and hyoid muscles during airway obstruction.

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.

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

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.

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

1988 ◽  
Vol 66 (5) ◽  
pp. 630-636 ◽  
Author(s):  
K. Ravi ◽  
K. K. Teo ◽  
C. T. Kappagoda
Keyword(s):  
Airway Pressure ◽  
Dynamic Compliance ◽  
Lymph Flow ◽  
Venous Congestion ◽  
Vascular Space ◽  
Airway Mechanics ◽  
Stretch Receptors ◽  
Pulmonary Stretch Receptors ◽  
Stimulation Of ◽  
Lymphatic Obstruction

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 extra vascular space.

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