Ozone-induced vagal reflex modulates airways reactivity in rabbits

Previous studies have demonstrated the efficacy of electroacupuncture at ST36 for patients with gastrointestinal motility disorders. While several lines of evidence suggest that the effect may involve vagal reflex, the precise molecular mechanism underlying this process still remains unclear. Here we report that the intragastric pressure increase induced by low frequency electric stimulation at ST36 was blocked by AP-5, an antagonist of N-methyl-D-aspartate receptors (NMDARs). Indeed, stimulating ST36 enhanced NMDAR-mediated, but not 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propanoic-acid-(AMPA-) receptor-(AMPAR-) mediated synaptic transmission in gastric-projecting neurons of the dorsal motor nucleus of the vagus (DMV). We also identified that suppression of presynapticμ-opioid receptors may contribute to upregulation of NMDAR-mediated synaptic transmission induced by electroacupuncture at ST36. Furthermore, we determined that the glutamate-receptor-2a-(NR2A-) containing NMDARs are essential for NMDAR-mediated enhancement of gastric motility caused by stimulating ST36. Taken together, our results reveal an important role of NMDA receptors in mediating enhancement of gastric motility induced by stimulating ST36.

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VAGAL REFLEX INFLUENCES ON CENTRAL RESPIRATORY CO-ORDINATION

Australian Journal of Experimental Biology and Medical Science ◽

10.1038/icb.1950.43 ◽

1950 ◽

Vol 28 (4) ◽

pp. 421-432 ◽

Cited By ~ 3

Author(s):

David IB Kerr

Keyword(s):

Vagal Reflex

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Childhood Asthma: Update

Pediatrics in Review ◽

10.1542/pir.13.11.403 ◽

1992 ◽

Vol 13 (11) ◽

pp. 403-412

Author(s):

Gail G. Shapiro

Keyword(s):

Smooth Muscle ◽

Mast Cells ◽

Airway Inflammation ◽

Immunoglobulin E ◽

Bronchial Hyperresponsiveness ◽

Basement Membrane Thickening ◽

Infiltrating Cells ◽

Lung Biopsies ◽

Airways Reactivity ◽

Mast Cell Mediator Release

Definition and Pathophysiology Asthma is a reversible airways disease characterized by both smooth muscle hyperreactivity and airway inflammation. During the 1970s and early 1980s the focus was on smooth muscle constriction, and it was believed that better bronchodilators would greatly diminish our difficulties in controlling this condition. This, unfortunately, was not the case. The emphasis of therapy today has turned to airway inflammation. Lung biopsies from patients who have asthma show destruction of respiratory epithelium, basement membrane thickening, and inflammatory cellular infiltrate. Among the infiltrating cells are eosinophils, macrophages, and neutrophils that are called to the site of inflammation by the chemotactic products released by activated mast cells. Upon their arrival, these cells release their own products of inflammation, which amplify this immunologic response. A variety of neuropeptides also play a role, some serving to stabilize and others to destabilize the airway. One result of this airway inflammation is airways reactivity, also known as bronchial hyperresponsiveness. A common example of this scenario is the child who has allergic asthma and encounters a problematic allergen. This child has immunoglobulin E (IgE) to this allergen bound to mast cells in his or her airway. Upon exposure to the allergen, the binding of IgE and antigen triggers mast cell mediator release within minutes.

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Electrophysiological-anatomic correlates of ATP-triggered vagal reflex in the dog. III. Role of cardiac afferents

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1996.270.5.h1785 ◽

1996 ◽

Vol 270 (5) ◽

pp. H1785-H1790 ◽

Cited By ~ 6

Author(s):

G. Katchanov ◽

J. Xu ◽

C. M. Hurt ◽

A. Pelleg

Keyword(s):

Carotid Artery ◽

Common Carotid Artery ◽

Left Common Carotid Artery ◽

Descending Aorta ◽

Chronotropic Action ◽

Vagal Reflex ◽

Vagal Afferent ◽

The Asymmetry ◽

Cardiac Afferents ◽

Afferent Terminals

To test the hypothesis that the asymmetry in the afferent traffic of the intra-right atrium (RA) ATP-triggered vagal reflex is due to the stimulation by ATP of extrapulmonary (i.e., cardiac) vagal chemosensitive afferent terminals, ATP, adenosine, and capsaicin were given into the canine RA and the aortic root (AR; n = 12); ATP and adenosine were also administered into the left common carotid artery and the descending aorta (n = 6). The negative chronotropic action [i.e., suppression of sinus node (SN) automaticity] of the test compounds and time to peak effect (tp) were determined. Under baseline conditions, ATP given into the left common carotid artery had a relatively very small effect. ATP given into the descending aorta had no effect. In contrast, intra-RA and intra-AR ATP markedly suppressed SN automaticity, the former less than the latter; the opposite was true for capsaicin. Intra-RA adenosine was much less potent than intra-RA ATP. The tp of intra-RA ATP and intra-RA adenosine were larger than the tp of intra-AR ATP. Pulmonary denervation did not alter the effects of intra-RAATP, intra-ARATP, or intra-AR capsaicin but almost abolished the effect of intra-RA capsaicin. Subsequent bilateral, but not left, cervical vagotomy markedly reduce the effects of ATP and eliminated the difference between the effects of ATP and adenosine. In addition, tp of intra-RA ATP and intra-AR ATP increased substantially and were similar to tp of adenosine. It was concluded that 1) ATP can stimulate vagal afferent terminals not only in the lungs but also in the heart, 2) the latter constitutes the vagal component of the negative chronotropic action of intra-RA or intra-AR ATP on SN automatically, and 3) the asymmetry in the vagal afferent traffic elicited by ATP in the heart (i.e., right vagal dominance) supersedes the symmetrical vagal afferent traffic triggered by intrapulmonary ATP.

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Perfusion of lung periphery: effects of local exposures to ozone and pressure

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.2.640 ◽

1986 ◽

Vol 61 (2) ◽

pp. 640-646

Author(s):

A. N. Freed ◽

U. A. Scheffel ◽

L. J. Kelly ◽

B. Bromberger-Barnea ◽

H. A. Menkes

Keyword(s):

High Pressure ◽

Pulmonary Perfusion ◽

Alveolar Pressure ◽

Anesthetized Dogs ◽

Lung Periphery ◽

Airways Reactivity ◽

Collateral System

Following ozone (O3) exposure, airways reactivity increases. We investigated the possibility that exposure to O3 causes a decrease in pulmonary perfusion, and that this decrease is associated with the increase in reactivity. Perfusion was measured with radiolabeled microspheres. A wedged bronchoscope was used to isolate sublobar segments in the middle and lower lobes of anesthetized dogs. Isolated segments were exposed to either O3 or an elevated alveolar pressure. Although increased alveolar pressure decreased microsphere density, exposure to 1 ppm O3 did not. Collateral system resistance rose significantly following exposure to O3 and to high pressure. These studies do not support the hypothesis that pulmonary perfusion is decreased following O3 exposure and is associated with subsequent increases in reactivity.

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Posterior cricoarytenoid and diaphragm activities during tidal breathing in neonates

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.5.1968 ◽

1988 ◽

Vol 64 (5) ◽

pp. 1968-1978 ◽

Cited By ~ 71

Author(s):

P. C. Kosch ◽

A. A. Hutchinson ◽

J. A. Wozniak ◽

W. A. Carlo ◽

A. R. Stark

Keyword(s):

Newborn Infants ◽

Emg Activity ◽

Time Interval ◽

Sudden Increase ◽

Tidal Breathing ◽

Term Neonates ◽

Dynamic Maintenance ◽

Sequential Activation ◽

Vagal Reflex ◽

Posterior Cricoarytenoid

To investigate airflow regulation in newborn infants, we recorded airflow, volume, diaphragm (Di), and laryngeal electromyogram (EMG) during spontaneous breathing in eight supine unsedated sleeping full-term neonates. Using an esophageal catheter electrode, we recorded phasic respiratory activity consistent with that of the principal laryngeal abductors, the posterior cricoarytenoids (PCA). Sequential activation of PCA and Di preceded inspiration. PCA activity typically peaked early in inspiration followed by either a decrescendo or tonic EMG activity of variable amplitude during expiration. Expiratory airflow retardation, or braking, accompanied by expiratory prolongation and reduced ventilation, was commonly observed. In some subjects we observed a time interval between PCA onset and a sudden increase in expiratory airflow just before inspiration, suggesting that release of the brake involved an abrupt loss of antagonistic adductor activity. Our findings suggest that airflow in newborn infants is controlled throughout the breathing cycle by the coordinated action of the Di and the reciprocal action of PCA and laryngeal adductor activities. We conclude that braking mechanisms in infants interact with vagal reflex mechanisms that modulate respiratory cycle timing to influence both the dynamic maintenance of end-expiratory lung volume and ventilation.

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