Laryngeal Regulation of Airway Resistance

1980 ◽  
Vol 89 (5) ◽  
pp. 462-466 ◽  
Author(s):  
Thomas V. McCaffrey ◽  
Eugene B. Kern
Keyword(s):  
Airway Resistance ◽  
Systemic Circulation ◽  
Regulation Of Respiration ◽  
Vagus Nerves ◽  
Receptor Stimulation ◽  
Lung Inflation ◽  
Pulmonary Receptor ◽  
Recurrent Laryngeal Nerves ◽  
Laryngeal Resistance ◽  
Stimulation Of

The response of laryngeal airway resistance to pulmonary receptor stimulation was studied in 20 mongrel dogs anesthetized with α-chloralose (80 mg/kg). Stimulation of pulmonary stretch receptors by lung inflation inhibited the phasic variation of laryngeal resistance during respiration and produced a sustained reduction of laryngeal resistance, which was related to lung inflation pressure. Stimulation of pulmonary J-receptors with capsaicin produced apnea and a large increase in laryngeal resistance. Capsaicin produced this reflex when injected into the pulmonary circulation but not when injected into the systemic circulation. Irritant receptor stimulation with histamine hydrochloride produced tachypnea and a reduction in inspiratory laryngeal resistance. Pulmonary receptor reflexes were abolished by dividing the vagus nerves distal to the origin of the recurrent laryngeal nerves. Laryngeal reflexes may be important in the regulation of respiration and the production of physiologic and pathologic alterations in pulmonary function.

Response of Laryngeal Airway Resistance to Chemoreceptor Stimulation: Effect of Pulmonary Afferent Denervation

1982 ◽  
Vol 90 (6) ◽  
pp. 723-727
Author(s):  
Thomas V. McCaffrey
Keyword(s):  
Airway Resistance ◽  
Afferent Input ◽  
Respiratory Neurons ◽  
Vagus Nerves ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Recurrent Laryngeal Nerves ◽  
Laryngeal Resistance ◽  
Stimulation Of ◽  
Laryngeal Airway

The response of laryngeal airway resistance to chemoreceptor stimulation was measured before and after vagotomy in ten anesthetized dogs. With the vagus nerves intact, stimulation of chemoreceptors produced a decrease in both inspiratory and expiratory laryngeal resistance. After bilateral vagotomy below the origin of the recurrent laryngeal nerves, stimulation of chemoreceptors produced a smaller decrease in inspiratory laryngeal resistance and an increase in expiratory laryngeal resistance. We concluded that pulmonary afferent input to the respiratory neurons maintains a low airway resistance during chemoreceptor stimulation.

Reflex Control of Nasal Blood Vessels

1987 ◽  
Vol 96 (3) ◽  
pp. 273-277 ◽  
Author(s):  
Shigeki Nishihira ◽  
Thomas V. Mccaffrey
Keyword(s):  
Blood Vessels ◽  
Nasal Mucosa ◽  
Vagus Nerves ◽  
Lung Inflation ◽  
Afferent Fibers ◽  
Reflex Arc ◽  
Capacitance Vessels ◽  
Nasal Blood Vessels ◽  
Pulmonary Stretch Receptor ◽  
Stimulation Of

The effect of stimulation of vagal afferent fibers on nasal blood vessels was studied in 36 cats. Volume change of the nasal capacitance vessels was measured by plethysmographic balloons inserted into the nose. Electrical stimulation of the vagus nerve produced a vasodilatation of nasal mucosa. Pulmonary stretch receptor stimulation by veratridine alkaloid and progressive lung inflation in open-chest cats also produced a vasodilatation of the nasal mucosa. These reflexes were abolished by sectioning the vagus nerves. These results suggest a reflex arc between the lung and nasal capacitance vessels which arises from pulmonary stretch receptors.

Effect of Chemoreceptor and Pulmonary Receptor Stimulation on Dilator Nares EMG Activity in the Dog

1983 ◽  
Vol 91 (6) ◽  
pp. 648-652 ◽  
Author(s):  
Daniel J. Blum ◽  
Thomas V. McCaffrey
Keyword(s):  
Upper Airway ◽  
Emg Activity ◽  
Receptor Stimulation ◽  
Lung Inflation ◽  
Anesthetized Dogs ◽  
Inspiratory Activity ◽  
Upper Airway Muscles ◽  
The Relationship ◽  
Pulmonary Stretch Receptor ◽  
Stimulation Of

To define the relationship between central control of upper airway muscles and respiratory muscle function, the electromyographic responses of the dilator nares muscles to stimulation of chemoreceptors and pulmonary receptors were studied in six anesthetized dogs. Only at maximal levels of hypoxia was the inspiratory activity of the dilator nares significantly increased. Hypercapnic stimulation increased the inspiratory activity with each incremental increase in CO2. Pulmonary stretch receptor stimulation produced by lung inflation inhibited dilator nares activity. Pulmonary irritant receptor stimulation by intravenously administered histamine increased dilator nares activity, as did pulmonary J receptor stimulation by the intravenous administration of capsaicin.

Respiratory pattern changes during costovertebral joint movement

1980 ◽  
Vol 48 (5) ◽  
pp. 862-867 ◽  
Author(s):  
R. Shannon
Keyword(s):  
Inhibitory Effect ◽  
Respiratory Pattern ◽  
Nerve Supply ◽  
Joint Movement ◽  
Receptor Stimulation ◽  
Lung Inflation ◽  
Manual Chest Compression ◽  
Costovertebral Joint ◽  
Spontaneously Breathing ◽  
Stimulation Of

Experiments were conducted to determine if costovertebral joint manipulation (CVJM) could influence the respiratory pattern. Phrenic efferent activity (PA) was monitored in dogs that were anesthetized with Dial-urethane, vagotomized, paralyzed, and artificially ventilated. Ribs 6-10 (bilaterally) were cut and separated from ribs 5-11. Branches of thoracic nerves 5-11 were cut, leaving only the joint nerve supply intact. Manual joint movement in an inspiratory or expiratory direction had an inhibitory effect on PA. Sustained displacement of the ribs could inhibit PA for a duration equal to numerous respiratory cycles. CVJM in synchrony with PA resulted in an increased respiratory rate. The inspiratory inhibitory effect of joint receptor stimulation was elicited with manual chest compression in vagotomized spontaneously breathing dogs, but not with artificial lung inflation or deflation. It is concluded that the effect of CVJM on the respiratory pattern is due to stimulation of joint mechanoreceptors, and that they exert their influence in part via the medullary-pontine rhythm generator.

scholarly journals Post-activation potentiation of gastric and intestinal contractions in response to stimulation of the vagus nerves

1959 ◽  
Vol 148 (2) ◽  
pp. 437-449 ◽  
Author(s):  
E. L. Blair ◽  
A. A. Harper ◽  
C. Kidd ◽  
T. Scratcherd
Keyword(s):  
Vagus Nerves ◽  
Stimulation Of

Dysfunction of M2-muscarinic receptors in pulmonary parasympathetic nerves after antigen challenge

1991 ◽  
Vol 71 (6) ◽  
pp. 2255-2261 ◽  
Author(s):  
A. D. Fryer ◽  
M. Wills-Karp
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Antigen Challenge ◽  
Saline Control ◽  
Control Group ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
Volume Blood ◽  
M2 Muscarinic Receptors ◽  
Stimulation Of

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

ANG II AT2 receptor modulates AT1receptor-mediated descending vasa recta endothelial Ca2+ signaling

2003 ◽  
Vol 284 (3) ◽  
pp. H779-H789 ◽  
Author(s):  
Kristie Rhinehart ◽  
Corey A. Handelsman ◽  
Erik P. Silldorff ◽  
Thomas L. Pallone
Keyword(s):  
Receptor Agonist ◽  
Calcium Concentration ◽  
Cyclopiazonic Acid ◽  
Receptor Activation ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Receptor Stimulation ◽  
Vasa Recta ◽  
Stimulation Of

We tested whether the respective angiotensin type 1 (AT1) and 2 (AT2) receptor subtype antagonists losartan and PD-123319 could block the descending vasa recta (DVR) endothelial intracellular calcium concentration ([Ca2+]i) suppression induced by ANG II. ANG II partially reversed the increase in [Ca2+]igenerated by cyclopiazonic acid (CPA; 10−5 M), acetylcholine (ACh; 10−5 M), or bradykinin (BK; 10−7 M). Losartan (10−5 M) blocked that effect. When vessels were treated with ANG II before stimulation with BK and ACh, concomitant AT2 receptor blockade with PD-123319 (10−8 M) augmented the suppression of endothelial [Ca2+]i responses. Similarly, preactivation with the AT2 receptor agonist CGP-42112A (10−8 M) prevented AT1 receptor stimulation with ANG II + PD-123319 from suppressing endothelial [Ca2+]i. In contrast to endothelial [Ca2+]i suppression by ANG II, pericyte [Ca2+]i exhibited typical peak and plateau [Ca2+]i responses that were blocked by losartan but not PD-123319. DVR vasoconstriction by ANG II was augmented when AT2 receptors were blocked with PD-123319. Similarly, AT2 receptor stimulation with CGP-42112A delayed the onset of ANG II-induced constriction. PD-123319 alone (10−5 M) showed no AT1-like action to constrict microperfused DVR or increase pericyte [Ca2+]i. We conclude that ANG II suppression of endothelial [Ca2+]i and stimulation of pericyte [Ca2+]i is mediated by AT1 or AT1-like receptors. Furthermore, AT2 receptor activation opposes ANG II-induced endothelial [Ca2+]i suppression and abrogates ANG II-induced DVR vasoconstriction.

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