Acute hypoxia prolongs the apnea induced by right atrial injection of capsaicin

2003 ◽  
Vol 94 (4) ◽  
pp. 1446-1454 ◽  
Author(s):  
Fadi Xu ◽  
Qi-Hai Gu ◽  
Tongrong Zhou ◽  
Lu-Yuan Lee
Keyword(s):  
Bolus Injection ◽  
Acute Hypoxia ◽  
Right Atrial ◽  
Ventilatory Responses ◽  
C Fibers ◽  
Bilateral Vagotomy ◽  
Prolonged Apnea ◽  
The Right ◽  
Spontaneously Breathing ◽  
Stimulation Of

Inspiratory central drive is augmented by acute hypoxia that leads to a hyperventilation, but it is inhibited by capsaicin (Cap)-induced stimulation of pulmonary C fibers (PCFs) that produces an expiratory apnea. We hypothesized that acute hypoxia should shorten or eliminate the Cap-induced apnea. The ventilatory responses to bolus injection of Cap (0.2–0.5 μg) into the right atrium before and during acute hypoxia (10% O2 for ∼1 min; Hypoxia+Cap) were compared in anesthetized and spontaneously breathing rats. We found that Cap injection during acute hypoxia produced an extremely long-lasting apnea (69.67 ± 11.97 s) that was 16-fold longer than the apnea induced by Cap alone (expiratory duration = 4.37 ± 0.53 s; P< 0.01). A similar prolonged apnea was also observed during hypoxia in anesthetized guinea pigs. Bilateral vagotomy abolished apneic responses to Cap both before and during hypoxia. Subsequent recording of single-fiber activity of PCFs (PCFA) showed that acute hypoxia did not significantly affect baseline PCFA but that it doubled PCFA responses to Cap via increasing both the firing rate (3.34 ± 0.76 to 7.65 ± 1.32 impulses/s; P < 0.05) and burst duration (1.12 ± 0.18 to 2.32 ± 0.31 s; P < 0.05). These results suggest that acute hypoxia augments PCF-mediated inspiratory inhibition and thereby leads to an extremely long-lasting apnea. This interaction is partially due to hypoxic sensitization of PCF response to Cap.

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.

Carotid sinus nerve is involved in cardiorespiratory responses to intracarotid injection of capsaicin in the rat

2006 ◽  
Vol 100 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Rurong Wang ◽  
Fadi Xu ◽  
Jianguo Zhuang ◽  
Cancan Zhang
Keyword(s):  
Carotid Sinus ◽  
Minute Ventilation ◽  
Right Atrial ◽  
Carotid Sinus Nerve ◽  
Cardiorespiratory Responses ◽  
C Fibers ◽  
Before And After ◽  
High Doses ◽  
The Right ◽  
Spontaneously Breathing

The carotid sinus nerve (CSN), important in cardiorespiratory modulation, mainly contains C fibers (CSCFs). Previous studies have demonstrated that selective stimulation of bronchopulmonary C fibers (PCFs) via right atrial injection of capsaicin (Cap; ∼0.25 μg) results in an apnea (∼3 s) associated with hypotension and bradycardia. The present study was undertaken to determine the effects of activating CSCFs on cardiorespiratory activities. Intracarotid injection of Cap was performed before and after bilateral transection of the CSN in anesthetized and spontaneously breathing rats. Our results showed that 1) low doses of Cap (up to 2 ng) produced an increase in minute ventilation by elevating both tidal volume and respiratory frequency with the threshold dosage at 1.0 ng ( P < 0.05); 2) high doses (4–64 ng) generated an apnea (prolongation of expiratory duration by ∼8-fold) and hypertension ( P < 0.05); 3) bilateral transection of the CSN reduced excitatory and inhibitory respiratory responses by 30 and 81%, respectively, and increased the hypertension by 88% ( P < 0.05); and 4) the same doses of Cap delivered into the right atrium to stimulate PCFs failed to evoke detectable cardiorespiratory responses. Our results suggest that compared with PCFs, CSCFs are more sensitive to Cap stimulation and that activation of these fibers significantly modulates cardiorespiratory activity in anesthetized rats.

scholarly journals 8-OH-DPAT abolishes the pulmonary C-fiber-mediated apneic response to fentanyl largely via acting on 5HT1A receptors in the nucleus tractus solitarius

2012 ◽  
Vol 303 (4) ◽  
pp. R449-R458 ◽  
Author(s):  
Jianguo Zhuang ◽  
Zhenxiong Zhang ◽  
Cancan Zhang ◽  
Fadi Xu
Keyword(s):  
Bolus Injection ◽  
Nucleus Tractus Solitarius ◽  
Right Atrial ◽  
Selective Blockade ◽  
C Fibers ◽  
5Ht1a Receptors ◽  
Way 100635 ◽  
Before And After ◽  
Μ Opioid Receptor ◽  
Spontaneously Breathing

Intravenous bolus injection of morphine causes a vagal-mediated brief apnea (∼3 s), while continuous injection, via action upon central μ-opioid receptor (MOR), arrests ventilation (>20 s) that is eliminated by stimulating central 5-hydroxytryptamine 1A receptors (5HT1ARs). Bronchopulmonary C-fibers (PCFs) are essential for triggering a brief apnea, and their afferents terminate at the caudomedial region of the nucleus tractus solitarius (mNTS) that densely expresses 5HT1ARs. Thus we asked whether the vagal-mediated apneic response to MOR agonists was PCF dependent, and if so, whether this apnea was abolished by systemic administration of 8-hydroxy-2-(di- n-propylamino)tetral (8-OH-DPAT) largely through action upon mNTS 5HT1ARs. Right atrial bolus injection of fentanyl (5.0 μg/kg, a MOR agonist) was performed in the anesthetized and spontaneously breathing rats before and after: 1) selective blockade of PCFs' conduction and subsequent bivagotomy; 2) intravenous administration of 5HT1AR agonist 8-OH-DPAT; 3) intra-mNTS injection of 8-OH-DPAT; and 4) intra-mNTS injection of 5HT1AR antagonist WAY-100635 followed by 8-OH-DPAT (iv). We found the following: First, fentanyl evoked an immediate apnea (2.5 ± 0.4 s, ∼6-fold longer than the baseline expiratory duration, TE), which was abolished by either blocking PCFs' conduction or bivagotomy. Second, this apnea was prevented by systemic 8-OH-DPAT challenge. Third, intra-mNTS injection of 8-OH-DPAT greatly attenuated the apnea by 64%. Finally, intra-mNTS microinjection of WAY-100635 significantly attenuated (58%) the apneic blockade by 8-OH-DPAT (iv). We conclude that the vagal-mediated apneic response to MOR activation depends on PCFs, which is fully antagonized by systemic 8-OH-DPAT challenge largely via acting on mNTS 5HT1ARs.

Fastigial nucleus-mediated respiratory responses depend on the medullary gigantocellular nucleus

2001 ◽  
Vol 91 (4) ◽  
pp. 1713-1722 ◽  
Author(s):  
Fadi Xu ◽  
Tongrong Zhou ◽  
Tonya Gibson ◽  
Donald T. Frazier
Keyword(s):  
Electrical Stimulation ◽  
Ibotenic Acid ◽  
Major Effect ◽  
Fastigial Nucleus ◽  
Respiratory Response ◽  
The Right ◽  
Spontaneously Breathing ◽  
Respiratory Responses ◽  
Gigantocellular Nucleus ◽  
Stimulation Of

Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 ± 11.0% ( P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 ± 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO2-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.

Endogenous BK stimulates ischemically sensitive abdominal visceral C fiber afferents through kinin B2 receptors

1994 ◽  
Vol 267 (6) ◽  
pp. H2398-H2406 ◽  
Author(s):  
H. L. Pan ◽  
G. L. Stahl ◽  
S. V. Rendig ◽  
O. A. Carretero ◽  
J. C. Longhurst
Keyword(s):  
Receptor Antagonist ◽  
Impulse Activity ◽  
Discharge Rate ◽  
Visceral Afferents ◽  
C Fibers ◽  
C Fiber ◽  
Hoe 140 ◽  
B2 Receptors ◽  
The Right ◽  
Stimulation Of

Abdominal ischemia and reperfusion reflexly activate the cardiovascular system. In the present study, we evaluated the role of endogenously produced bradykinin (BK) in the stimulation of ischemically sensitive visceral afferents. Single-unit activity of abdominal visceral C fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats during 5 min of abdominal ischemia. Abdominal ischemia increased the portal venous plasma BK level from 49 +/- 10 to 188 +/- 66 pg/ml (P < 0.05). Injection of BK (1 microgram/kg ia) into the descending aorta significantly increased impulse activity (0.88 +/- 0.16 impulses/s) of 10 C fibers, whereas a kinin B1-receptor agonist, des-Arg9-BK (1 microgram/kg), did not alter the discharge rate. Inhibition of kininase II activity with captopril (4 mg/kg i.v.) potentiated impulse activity of 14 ischemically sensitive C fibers (0.44 +/- 0.09 vs. precaptopril, 0.33 +/- 0.08 impulses/s; P < 0.05). In addition, a kinin B2-receptor antagonist (NPC-17731; 40 micrograms/kg i.v.) attenuated activity of afferents during ischemia (0.39 +/- 0.08 vs. pre-NPC-17731, 0.72 +/- 0.13 impulses/s; P < 0.05) and eliminated the response of 10 C fibers to BK. Another kinin B2-receptor antagonist, Hoe-140 (30 micrograms/kg iv), had similar inhibitory effects on six other ischemically sensitive C fibers. In 15 separate cats treated with aspirin (50 mg/kg i.v.), Hoe-140 (30 micrograms/kg i.v.) attenuated impulse activity of only 3 of 16 ischemically sensitive C fibers. These data suggest that BK produced during abdominal ischemia contributes to the stimulation of ischemically sensitive visceral C fiber afferents through kinin B2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Postnatal development of right atrial injection of capsaicin-induced apneic response in rats

2006 ◽  
Vol 101 (1) ◽  
pp. 60-67 ◽  
Author(s):  
Rurong Wang ◽  
Fadi Xu
Keyword(s):  
Respiratory Failure ◽  
Postnatal Development ◽  
Pulmonary Disease ◽  
Bolus Injection ◽  
Right Atrial ◽  
Newborn Rats ◽  
Respiratory Dysfunction ◽  
Percent Change ◽  
C Fiber ◽  
Spontaneously Breathing

Apnea and respiratory failure often occur in infants with pulmonary disease. Bronchopulmonary C-fiber (PCF)-mediated apnea is an important component of respiratory dysfunction. This study was undertaken to define the postnatal development of PCF-mediated apnea. The experiments were conducted in five groups of anesthetized, tracheotomized, and spontaneously breathing rats with ages at postnatal days P1–3, P7–9, P14–16, P21–23, and P56–58. Right atrial bolus injection of three doses of capsaicin (Cap), equivalent to 2, 4, and 8 μg/kg used previously in 450-g rats, was applied to stimulate PCFs. We found that 1) Cap-induced apneic response [percent change from the baseline expiratory duration (Te) values (ΔTe%)] and the sensitivity of this response (ΔTe%·μg−1) were significantly greater in the rats <P10 than those >P10; 2) the Cap-induced apneas were vagally dependent in all rats tested; and 3) bivagotomy-induced prolongation of Te was much greater in the rats <P10 than those >P10. From these findings we concluded that, compared with the older rats (>P10), the newborn rats have a stronger PCF-mediated respiratory inhibition that may contribute to infants' vulnerability to respiratory failure.

Effect of cervical vagal stimulation on chicken heart rate and atrioventricular conduction

1983 ◽  
Vol 244 (2) ◽  
pp. R235-R243
Author(s):  
J. M. Goldberg ◽  
M. H. Johnson ◽  
K. D. Whitelaw
Keyword(s):  
Heart Rate ◽  
Vagal Stimulation ◽  
Atrioventricular Conduction ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Chicken Heart ◽  
Av Conduction ◽  
Supramaximal Stimulation ◽  
The Right ◽  
Stimulation Of

The effects of supramaximal stimulation of the right and left cervical vagi on heart rate, pacemaker localization, and atrioventricular (AV) conduction were investigated in 15 anesthetized open-chest chickens before and after atropine sulfate. Epicardial bipolar electrograms were recorded from selected atrial sites and right ventricle. A back lead electrocardiogram was also recorded. The effect of stimulation on atrioventricular conduction was evaluated during pacing from one of the right atrial recording sites. Supramaximal stimulation of either cervical vagus produced bradycardia but not cardiac arrest. Heart rate was reduced from an average spontaneous rate of 282 +/- 13 (SE)/min to 161 +/- 13/min with stimulation of the right and left cervical vagus. Pacemaker shifts occurred in over 50% of the vagal stimulations. The most frequent shift occurred to the lower AV node or ventricles. Pacemaker shifts to the AV junctional region producing almost simultaneous activation of the atria and ventricles were not observed. Vagal stimulation during atrial pacing produced minimal prolongation in AV conduction time [right vagus, 13 +/- 3 (SE) ms; left vagus, 8 +/- 2 ms]. Second and third degree heart blocks were not observed during pacing. Vagal stimulation after atropine indicates that the cervical vagi do not contain sympathetic fibers going to pacemaker or AV conduction tissues.

Metoclopramide blocks the phenyl diguanide and 5-hydroxytryptamine induced cardiorespiratory reflexes in cats and dogs

1988 ◽  
Vol 66 (6) ◽  
pp. 776-782 ◽  
Author(s):  
K. Ravi ◽  
N. B. Dev
Keyword(s):  
Left Atrial ◽  
Right Atrial ◽  
Excitatory Effect ◽  
Reflex Responses ◽  
Cardiorespiratory Responses ◽  
C Fiber ◽  
Spontaneously Breathing ◽  
Cardiac Receptors ◽  
Sensory Endings ◽  
Stimulation Of

The effects of metoclopramide on the reflex cardiorespiratory responses elicited by stimulation of pulmonary J receptors by right atrial injections of phenyl diguanide (PDG), 5-hydroxytryptamine (5-HT), and capsaicin were investigated in anesthetized spontaneously breathing cats. It was observed that while metoclopramide blocked the responses to PDG and 5-HT injections, it spared the responses to capsaicin injections. Similarly, metoclopramide was without effect on the reflex responses following activation of pulmonary C-fiber receptors (J receptors) by capsaicin in dogs. Reflex cardiorespiratory responses elicited by left atrial injections of PDG and 5-HT, owing to stimulation of cardiac receptors in cats, and reflex responses following right or left atrial injections of PDG and 5-HT, owing to stimulation of aortic chemoreceptors in dogs, were also found to be blocked by metoclopramide. Afferent impulse activity recorded from aortic chemoreceptors of dogs showed that while metoclopramide depressed the excitatory effect of PDG and 5-HT on them, it did not produce any effect on their spontaneous activity and their excitation by hypoxia. The results from the reflex studies show that metoclopramide is capable of antagonizing the reflex responses following the activation of the cardiopulmonary afferents by PDG and 5-HT. Based on the effects on aortic chemoreceptor afferents, it is suggested that PDG, 5-HT, and metoclopramide may be acting upon the regenerative region of the sensory endings.

"Summation" of the increase in heart rate from stimulation of atrial receptors

1980 ◽  
Vol 58 (6) ◽  
pp. 666-672
Author(s):  
P. V. Greenwood ◽  
C. T. Kappagoda
Keyword(s):  
Heart Rate ◽  
Left Atrial ◽  
Superior Vena ◽  
Right Atrial ◽  
Propranolol Hydrochloride ◽  
Superior Vena Caval ◽  
The Right ◽  
Atrial Receptors ◽  
Stimulation Of ◽  
Wire Cage

In dogs anaesthetized with chloralose, application of stimuli which are likely to activate left atrial (L.A.) and right atrial (R.A.) receptors (complex unencapsulated endings) has been shown to result in an increase in heart rate. The present investigation was undertaken to determine whether the response elicited by the application of one stimulus (i.e., to the left atrium) could be enhanced by the application of a second stimulus (i.e., to the right atrium) in the same animal.The L.A. receptors were stimulated by distending a small balloon at the right upper pulmonary vein-L.A. junction and the R.A. receptors by "expanding" a spherical wire cage positioned at the superior vena caval (S.V.C.)-R.A. junction. Pressures in the S.V.C., R.A., L.A., and femoral artery were measured and the electrocardiogram monitored.In eight dogs stimulation of L.A. receptors resulted in an increase in heart rate (H.R.) of 18.5 beats/min (SEM 6.0; N = 23). In the same animals stimulation of R.A. receptors resulted in an increase in H.R. of 14.6 beats/min (SEM 2.0; N = 25). Application of both stimuli simultaneously resulted in an increase of 32.2 beats/min (SEM 8.0; N = 13). In four dogs propranolol hydrochloride (0.5 mg/kg) markedly diminished the response. In three dogs the response was abolished by bretylium tosylate (10 mg/kg).It is concluded that the increase in H.R. resulting from the application of these two stimuli could be "summated" and these findings support the proposition that the receptors in the two atria act as a functional entity.

scholarly journals INFLUENCE OF PERMANENT PACING OF THE ATRIA FROM UPPER ANTERIOR AREA OF INTERCARDIAC SEPTA (AREA OF BAKHMAN’S FASCICLES) ON THE PART OF AMOTIVATIONAL VENTRICLE STIMULATION

2016 ◽  
Vol 175 (2) ◽  
pp. 12-16
Author(s):  
M. V. Didenko ◽  
G. S. Pasenov ◽  
G. G. Khubulava
Keyword(s):  
Right Ventricle ◽  
Sinus Node ◽  
Right Atrial ◽  
Permanent Pacing ◽  
Ventricular Stimulation ◽  
The Right ◽  
Stimulation Of

This research includes 74 patients with syndrome of the sinus node asthenia. The application of permanent bilocular pacing was indicated for these patients. An atrial electrode was located in the right atrial auricle in 37 patients and it was in the area of Bakhman’s fascicles in other 37 patients. All the patients had a stimulated atrio-ventricular delay on 250 ms, but sensing delay was shorter on 20 ms. Given data were analyzed after operation in the periods of 6 and 12 months. Cumulative percent of ventricular stimulation was significantly less in the group with electrode in the area of Bakhman’s fascicles (6%) as compared with the group where electrode installed in the right atrial auricle (41%) after 6 months. There were 4% in comparison with 43% after 12 months. The localization of atrial electrode in the area of Bakhman’s fascicles led to reduction of cumulative percent of ventricular stimulation on 35% after 6 months and on 39% after 12 months. Permanent pacing in the area of Bakhman’s fascicles could be an effective mode to decrease the part of amotivational stimulation of the right ventricle.

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