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

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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Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.3.765 ◽

1997 ◽

Vol 82 (3) ◽

pp. 765-771 ◽

Cited By ~ 17

Author(s):

H. F. Chen ◽

B. P. Lee ◽

Y. R. Kou

Keyword(s):

Hydroxyl Radical ◽

Right Atrium ◽

Air Embolism ◽

Lung Mechanics ◽

Cyclooxygenase Inhibitor ◽

Functional Importance ◽

C Fibers ◽

The Right ◽

Saline Vehicle ◽

Stimulation Of

Chen, H. F., B. P. Lee, and Y. R. Kou. Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs. J. Appl. Physiol. 82(3): 765–771, 1997.—We investigated the involvement of the cyclooxygenase metabolites and hydroxyl radical (⋅ OH) in the stimulation of vagal pulmonary C fibers (PCs) by pulmonary air embolism (PAE). Impulses were recorded from PCs in 51 anesthetized, open-chest, and artificially ventilated dogs. Fifty of 59 PCs were stimulated by infusion of air into the right atrium (0.2 ml ⋅ kg−1 ⋅ min−1for 10 min). As a group ( n = 59), PC activity increased from a baseline of 0.4 ± 0.1 to a peak of 1.7 ± 0.2 impulses/s during the period from 1 min before to 2 min after the termination of PAE induction. In PCs initially stimulated by PAE induction, PAE was repeated after the intervening treatment (iv) with saline ( n = 9), ibuprofen (a cyclooxygenase inhibitor; n = 11), or dimethylthiourea (a ⋅ OH scavenger; n = 12). The responses of PCs to PAE were not altered by saline vehicle but were abolished by ibuprofen and significantly attenuated by dimethylthiourea. Although hyperinflation of the lungs reversed the PAE-induced bronchomotor responses, it did not reverse the stimulation of PCs ( n= 8). These results suggest that 1) cyclooxygenase products are necessary for the stimulation of PCs by PAE, whereas changes in lung mechanics are not, and 2) the functional importance of cyclooxygenase products may be mediated in part through the formation of ⋅ OH.

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Reflex tracheal contraction evoked in dogs by bronchodilator prostaglandins E2 and I2

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.6.1823 ◽

1985 ◽

Vol 58 (6) ◽

pp. 1823-1831 ◽

Cited By ~ 46

Author(s):

A. M. Roberts ◽

H. D. Schultz ◽

J. F. Green ◽

D. J. Armstrong ◽

M. P. Kaufman ◽

...

Keyword(s):

General Circulation ◽

Bronchial Artery ◽

Human Subjects ◽

Muscle Tension ◽

C Fibers ◽

Anesthetized Dogs ◽

Vagal Reflex ◽

Afferent Vagal ◽

Vagal Cooling ◽

Airway Irritation

Bronchodilator prostaglandins E2 and I2 may cause airway irritation and bronchoconstriction in human subjects. These experiments were designed to test the hypothesis that this paradoxical bronchoconstriction is a vagal reflex triggered by stimulation of airway afferents. We recorded smooth muscle tension in an innervated upper tracheal segment in anesthetized dogs and injected prostaglandins into the general circulation or into a bronchial artery or administered them as aerosol to the lungs. Prostaglandins usually caused tracheal contraction, which survived vagal cooling to 5–7 degrees C but was abolished at 0 degrees C. Vagally mediated tracheal contraction was also evoked when prostacyclin was injected into the pulmonary circulation of dogs whose pulmonary and systemic circulations were independently pump perfused. Recordings of afferent vagal impulses indicated that bronchial arterial injection of prostaglandins stimulated bronchial C-fibers; aerosols of prostaglandin stimulated pulmonary and bronchial C-fibers and C-fibers in extrapulmonary airways. We postulate that in susceptible human subjects concentrations of these prostaglandins too low to have direct bronchodilator effects may cause reflex bronchoconstriction by stimulating afferent vagal C-fibers in the lower airways.

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Vagal C-fiber blockade abolishes sympathetic inhibition by atrial natriuretic factor

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1988.255.1.r6 ◽

1988 ◽

Vol 255 (1) ◽

pp. R6-R13 ◽

Cited By ~ 9

Author(s):

H. D. Schultz ◽

D. G. Gardner ◽

C. F. Deschepper ◽

H. M. Coleridge ◽

J. C. Coleridge

Keyword(s):

Atrial Natriuretic Factor ◽

Splanchnic Nerve ◽

Nerve Activity ◽

Renal Nerve ◽

C Fibers ◽

Natriuretic Factor ◽

Anesthetized Rats ◽

Renal Nerve Activity ◽

Afferent Vagal ◽

Atrial Natriuretic

Administration of atrial natriuretic factor (ANF) to anesthetized rats decreases renal nerve activity (RNA), an effect prevented by vagotomy but not by atropine. We sought to determine whether afferent vagal C-fibers mediate the inhibition of sympathetic outflow. ANF (2.5 micrograms/kg iv) decreased mean arterial pressure (MAP) by 25 +/- 2 mmHg, RNA by 11 +/- 5%, and least splanchnic nerve activity (LSNA) by 10 +/- 4% in anesthetized rats with arterial baroreceptors intact, and by 40 +/- 3 mmHg, 28 +/- 7%, and 23 +/- 4%, respectively, in sinoaortic-denervated rats. Inhibition of RNA and LSNA by ANF was reduced slightly by cooling the vagi to 6 or 7 degrees C, a temperature at which conduction in A-fibers was blocked and that in C-fibers attenuated; inhibition was abolished when C-fibers were blocked by cooling to 0 degrees C. We conclude that the inhibition of RNA and LSNA by ANF was mediated by afferent vagal C-fibers. We also obtained evidence that the aortic nerves contribute to ANF-induced inhibition of RNA. Our results support the notion that ANF evokes a generalized decrease in sympathetic tone that contributes to the hypotension, cardiac inhibition, and natriuresis accompanying systemic administration of the peptide.

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Pulmonary rapidly adapting receptors reflexly increase airway secretion in dogs

Journal of Applied Physiology ◽

10.1152/jappl.1989.67.2.682 ◽

1989 ◽

Vol 67 (2) ◽

pp. 682-687 ◽

Cited By ~ 38

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.

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

Journal of Applied Physiology ◽

10.1152/jappl.1993.74.5.2345 ◽

1993 ◽

Vol 74 (5) ◽

pp. 2345-2352 ◽

Cited By ~ 70

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.

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Phenyl biguanide does not inhibit locomotion in conscious rabbits

Journal of Applied Physiology ◽

10.1152/jappl.1995.79.4.1346 ◽

1995 ◽

Vol 79 (4) ◽

pp. 1346-1350 ◽

Cited By ~ 1

Author(s):

K. P. O'Hagan ◽

R. S. Anderson ◽

L. B. Bell ◽

S. W. Mittelstadt ◽

P. S. Clifford

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

New Zealand ◽

Saline Infusion ◽

C Fibers ◽

New Zealand White Rabbits ◽

Saline Vehicle ◽

Cardiac Receptors ◽

Respiratory Responses ◽

Stimulation Of

Stimulation of cardiopulmonary vagal C fibers with phenyl biguanide (PBG) reflexly inhibits locomotion in addition to causing depression of blood pressure (BP), heart rate (HR), and respiration in cats and rats. We investigated whether PBG caused somatomotor inhibition during exercise in the rabbit, a species in which it is known that the hemodynamic and respiratory responses to PBG are mediated by cardiac rather than by pulmonary receptors. In eight New Zealand White rabbits, BP, HR, and hindlimb electromyographic (EMG) responses to 60 and 120 micrograms/kg PBG and saline vehicle were evaluated during two separate 3-min exercise bouts at 10 m/min at 0% grade. During exercise, 60 micrograms/kg PBG decreased BP (-27 +/- 4 mmHg) and HR (-95 +/- 16 beats/min) but did not inhibit locomotion as suggested by the EMG response (+112 +/- 8% of preinfusion EMG). Hemodynamic and EMG responses to 120 micrograms/kg PBG were similar to 60 micrograms/kg PBG. Saline infusion during exercise had no effect on HR, BP, or locomotion (+114 +/- 8% of preinfusion EMG). Locomotion is not inhibited by PBG in rabbits, which suggests that PBG-induced reflex somatomotor inhibition observed in other species is primarily mediated by pulmonary rather than by cardiac receptors.

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