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.

Pattern of Cardiorespiratory Afferent Convergence to Solitary Tract Neurons Driven by Pulmonary Vagal C-Fiber Stimulation in the Mouse

1998 ◽  
Vol 79 (5) ◽  
pp. 2365-2373 ◽  
Author(s):  
Julian F. R. Paton
Keyword(s):  
Respiratory Activity ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Solitary Tract ◽  
C Fibers ◽  
C Fiber ◽  
Central Respiratory Activity ◽  
Fiber Stimulation ◽  
Cardiac Receptors ◽  
Stimulation Of

Paton, Julian F. R. Pattern of cardiorespiratory afferent convergence to solitary tract neurons driven by pulmonary vagal C-fiber stimulation in the mouse. J. Neurophysiol. 79: 2365–2373, 1998. The central integration of signals from pulmonary vagal C-fibers (or type-J receptors) with those arising from cardiac, peripheral chemoreceptor, and baroreceptor afferents to neurons within the nucleus of the solitary tract (NTS) was studied in an arterially perfused working heart–brain stem preparation of adult mouse. Pulmonary vagal C-fibers were excited by right atrial injection of phenylbiguanide (PBG) while cardiac receptors were stimulated by left ventricular injection of veratridine (1–3 μg/kg) or mechanically by distension of the left ventricle (20–50 μl perfusate) using an indwelling cannula. Carotid body chemoreceptors were activated by aortic injection of Na cyanide, whereas baroreceptors were stimulated by increasing arterial perfusion pressure. Stimulation of pulmonary C-fibers and cardiac, chemo-, and baroreceptors all produced a reflex bradycardia (23–133 bpm). Central respiratory activity, as recorded from the phrenic nerve, was depressed by stimulating pulmonary C-fibers and cardiac and baroreceptors but enhanced in amplitude and frequency during chemoreceptor stimulation. Twenty-seven NTS neurons were excited and three were inhibited after pulmonary C-fiber stimulation displaying decrementing discharges with a peak firing frequency of up to 42 Hz (15 ± 2.2 Hz, mean ± SE) that lasted for 8.8 ± 0.9 s. These responses occurred <1 s from the end of the PBG injection that was within the pulmonary circulation time. None of these cells responded to increases in right atrial pressure. All cells excited by PBG were also driven synaptically after electrical stimulation of the ipsilateral cervical vagus nerve at a latency of 32.9 ± 3.2 ms (range 20–62 ms). None of these neurons had ongoing activity related to central respiratory activity. Convergence from cardiorespiratory afferents to 21 neurons driven by pulmonary C-fibers was tested. Twenty-five percent of cells were selectively excited by chemical stimulation of cardiac receptors alone, 19% were driven by peripheral chemoreceptors, and 38% responded to both cardiac and chemoreceptor activation. In contrast, only 13% of the cells activated by PBG injection responded to stimulation of baroreceptors and only 6% to cardiac mechanoreceptor stimulation. None of these neurons were activated by increasing right atrial pressure. The data indicate a high proportion of afferent convergence from pulmonary C-fibers, cardiac receptors, and peripheral chemoreceptors in the NTS. However, these neurons appear not to integrate inputs from cardiovascular mechanoreceptors. The significance of the data is discussed in relation to pathological disease states such as pulmonary congestion and cardiac failure.

Effect of hypoxia on reflex responses of tracheal submucosal glands

1995 ◽  
Vol 78 (5) ◽  
pp. 1651-1656 ◽  
Author(s):  
R. Hejal ◽  
K. P. Strohl ◽  
B. Erokwu ◽  
N. S. Cherniack ◽  
M. A. Haxhiu
Keyword(s):  
Right Atrial ◽  
Liquid Droplets ◽  
Submucosal Gland ◽  
Response Curves ◽  
Reflex Responses ◽  
Hyperoxic Condition ◽  
Airway Secretion ◽  
Calculated Volume ◽  
Lung Deflation ◽  
Stimulation Of

The effects of moderate sustained normocapnic hypoxia on tracheal submucosal gland reflex responses were studied. Experiments were performed in anesthetized, paralyzed, and mechanically ventilated dogs. The changes in the number of secreting glands and volume of secreted fluid in the subsequent period of time were recorded after 15–30 min of controlled ventilation with room air [arterial PO2 (PaO2) 86 +/- 3 Torr], hypoxic gas mixture (PaO2 49 +/- 4 Torr), or 100% O2 (PaO2 339 +/- 39 Torr), under isocapnic and isohydric conditions. The hillocks method was used to quantify the changes in submucosal gland secretion. The changes in secretion 30 s after stimulation of pulmonary C-fiber receptors by right atrial injection of capsaicin (10 micrograms/kg; n = 10) were markedly lower during moderate hypoxia than in normoxia or hyperoxia. Differences in the number of liquid droplets and the volume of secreted fluid were statistically significant (P < 0.05 and P < 0.001, respectively). Stimulation of airway rapidly adapting receptors by lung deflation increased airway secretion; the number of “hillocks” and the volume of secreted fluid were lower in hypoxic than in hyperoxic state. Differences between response curves for the number of glands activated and secreted volume were statistically significant (P < 0.05 and P < 0.001). The number of glands activated by substance P given locally by arterial infusion was not affected by the state of oxygenation, but the calculated volume of secreted fluid was lower during the hypoxic state than under hyperoxic condition (P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

"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.

Convergence Properties of Solitary Tract Neurons Responsive to Cardiac Receptor Stimulation in the Anesthetized Cat

1998 ◽  
Vol 79 (5) ◽  
pp. 2374-2382 ◽  
Author(s):  
L. Silva-Carvalho ◽  
J.F.R. Paton ◽  
I. Rocha ◽  
G. E. Goldsmith ◽  
K. M. Spyer
Keyword(s):  
Carotid Sinus ◽  
Right Atrial ◽  
Solitary Tract ◽  
Convergence Properties ◽  
Receptor Stimulation ◽  
Carotid Chemoreceptors ◽  
C Fibers ◽  
Cardiac Receptors ◽  
Stimulation Of ◽  
Anesthetized Cat

Silva-Carvalho, L., J.F.R. Paton, I. Rocha, G. E. Goldsmith and K. M. Spyer. Convergence properties of solitary tract neurons responsive to cardiac receptor stimulation in the anesthetized cat. J. Neurophysiol. 79: 2374–2382, 1998. The convergence pattern of cardiac receptors, pulmonary C-fibers, carotid chemoreceptor, and baroreceptor afferents onto neurons within the nucleus of the solitary tract (NTS) was studied in the anesthetized (pentobarbitone sodium, 40 mg/kg,) paralyzed and artificially ventilated cat. Extra- and intracellular recordings were made from NTS neurons while stimulating both cardiac receptors by aortic root injections of veratridine (1–3 μg/kg) and pulmonary C-fibers by a right atrial injection of phenylbiguanide (10–20 μg/kg). The ipsilateral carotid body was stimulated by using arterial injection of CO2-saturated bicarbonate solution, whereas inflation of the ipsilateral carotid sinus was used to activate baroreceptors. The ipsilateral cardiac vagal branch, cervical vagus, and carotid sinus nerves were stimulated electrically (1 Hz, 0.2–1 ms, 1–35 V). In 78 NTS neurons recorded either extracellularly ( n = 47) or intracellularly ( n = 31), electrical stimulation of the cardiac branch of the vagus nerve evoked synaptic potentials (spikes and/or excitatory postsynaptic potentials) with an onset latency between 4 and 220 ms. Some neurons displayed both short and long latency inputs(15.5 ± 1.8 and 160.0 ± 8.5 ms; n = 14). Of these 78 neurons, 24 responded to veratridine stimulation of cardiac receptors (i.e., cardioreceptive neurons) by exhibiting an augmenting–decrementing discharge of 37 ± 4 s in duration with a peak frequency of 30 ± 5 Hz. Convergence from other cardiorespiratory receptors was noted involving either carotid chemoreceptors ( n = 7) or pulmonary C-fibers ( n = 4) or from both carotid chemoreceptors and pulmonary C-fibers ( n = 6). In contrast, only one cardioreceptive NTS neuron was activated by distension of the carotid sinus. Recording sites recovered were confined to the medial NTS at the level of the area postrema and extended caudally into the commissural subnucleus. Our results indicate a convergence of carotid chemoreceptor and pulmonary C-fiber afferent inputs to cardioreceptive NTS neurons. With the paucity of baroreceptor inputs to these neurons it is suggested that sensory integration within the NTS may reflect regulatory versus defensive or protective reflex control.

Cardiac responses to electrical stimulation of discrete loci in canine atrial and ventricular ganglionated plexi

1990 ◽  
Vol 259 (5) ◽  
pp. H1365-H1373 ◽  
Author(s):  
C. K. Butler ◽  
F. M. Smith ◽  
R. Cardinal ◽  
D. A. Murphy ◽  
D. A. Hopkins ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Right Ventricular ◽  
Left Atrial ◽  
Right Atrial ◽  
Intramyocardial Pressure ◽  
Cardiac Responses ◽  
Ganglionated Plexi ◽  
The Right ◽  
Ganglionated Plexus ◽  
Stimulation Of

The purpose of the present study was to examine cardiac effects induced by electrical stimulation (1-4 V, 1 ms, 200 Hz) of discrete loci within the ganglionated plexi located on canine atria and ventricles. When 20 loci in the right atrial ventral ganglionated plexi of 11 anesthetized open-chest dogs were stimulated, bradycardia and/or right and left atrial force suppression occurred when, on average, 15% of these loci were stimulated. Bradycardia and atrial force suppression were elicited when, on average, 8% of 15 loci in the left atrial ventral ganglionated plexi of eight dogs was stimulated. When these loci were restimulated after acute decentralization, cardiac responses were attenuated or occasionally eliminated. After atropine (1 mg/kg iv) administration, repeat stimulation of loci in the right but not left atrial ganglionated plexus induced tachycardia. Stimulation of loci in the right ventricular ganglionated plexus after the subsequent administration of desipramine (1 mg/kg iv) in six dogs resulted in an increase in right ventricular conus intramyocardial pressure. After hexamethonium administration (10 mg/kg iv, followed by a continuous infusion of 1 mg.kg-1.min-1), sympathetic responses were no longer elicited from one of the five dogs in which loci in the right atrial ganglionated plexi and from two of the six dogs in which loci of the right ventricular ganglionated plexus had elicited responses. We conclude that atrial and ventricular ganglionated plexi contain efferent parasympathetic, efferent sympathetic, and afferent neurons.

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.

Cardiovascular afferent signals and drinking in response to hypotension in dogs

1999 ◽  
Vol 277 (3) ◽  
pp. R795-R801 ◽  
Author(s):  
Terry N. Thrasher ◽  
Craig R. Keenan ◽  
David J. Ramsay
Keyword(s):  
Pulmonary Artery ◽  
Water Intake ◽  
Left Atrial ◽  
Inferior Vena ◽  
Vena Cava ◽  
Ascending Aorta ◽  
Right Atrial ◽  
Arterial Hypotension ◽  
Atrial Receptors ◽  
Stimulation Of

Arterial hypotension stimulates increases in plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake in conscious dogs. We have previously reported that increasing left atrial but not right atrial pressure completely blocks the increase in plasma AVP and PRA induced by hypotension. The goal of the present study was to examine the effect of increasing right or left atrial pressure on water intake induced by arterial hypotension. Dogs were prepared with occluding cuffs on the thoracic inferior vena cava, the pulmonary artery, and the ascending aorta. We reduced mean arterial pressure (MAP) 25% below control by either inferior vena cava constriction (IVCC), pulmonary artery constriction (PAC), or ascending aorta constriction (AAC) and measured water intake over a 2-h period. Cumulative water intake during IVCC ( n = 6) and PAC ( n = 6) was 7.8 ± 2.0 and 6.7 ± 2.6 ml/kg, respectively. There was no difference between either the latency or the volume consumed between the two treatments. In contrast, none of the dogs drank during hypotension induced by AAC ( n = 5). Because the degree of arterial baroreceptor unloading was the same in each treatment by design, we conclude that stimulation of left atrial receptors inhibits drinking in response to arterial hypotension but that stimulation of right atrial receptors has no effect on the response in dogs.

Responses to activation of cardiac sympathetic afferents with epicardial bradykinin

1982 ◽  
Vol 242 (2) ◽  
pp. H148-H153 ◽  
Author(s):  
R. B. Felder ◽  
M. D. Thames
Keyword(s):  
Left Ventricular ◽  
Renal Sympathetic Nerve Activity ◽  
Reflex Responses ◽  
Cardiovascular Reflex ◽  
Afferent Fibers ◽  
Excitatory Responses ◽  
Cardiac Receptors ◽  
Sensory Endings ◽  
Renal Sympathetic ◽  
Biphasic Responses

The cardiovascular reflex responses mediated by cardiac sympathetic afferent fibers (CSA) appear to differ depending on the nature of the activating stimulus. Although electrical stimulation of CSA may result in either excitatory of inhibitory reflex responses in both cats and dogs, topical application of bradykinin to these sensory endings elicits only excitatory reflex responses in cats. The present experiments were performed to determine whether CSA activated by epicardial bradykinin also mediate solely excitatory reflex responses in the dog. The changes in efferent cardiac or renal sympathetic nerve activity, mean arterial pressure, and heart rate resulting from application of bradykinin to the left ventricular epicardial surface were determined in 15 chloralose-anesthetized, sinoaortic-denervated vagotomized dogs. Activation of CSA with bradykinin (0.1—120 g/ml) elicited inhibitory responses in eight dogs, excitatory responses in four dogs, and biphasic responses in three dogs. Both excitatory and inhibitory reflexes were eliminated by cardiac sympathetic afferent denervation. The results show that, in the dog, cardiac receptors with sympathetic afferent fibers activated by epicardial bradykinin mediate nonuniform reflex responses that tend to be predominantly inhibitory.

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