Reflex circulatory changes due to the afferent stimulation of cat pericoronary nerve

1978 ◽  
Vol 235 (6) ◽  
pp. H759-H766
Author(s):  
T. Shimizu ◽  
D. F. Peterson ◽  
V. S. Bishop
Keyword(s):  
Sympathetic Nerves ◽  
Heart Rate Change ◽  
Vagal Afferents ◽  
Depressor Response ◽  
Efferent Pathway ◽  
C Fibers ◽  
Pressor Reflex ◽  
Circulatory Reflexes ◽  
The Right ◽  
Stimulation Of

Two different types of circulatory reflexes evoked by electrical stimulation of afferent fibers in the left pericoronary nerves were studied in anesthetized cats. A depressor response (-32.5 mmHg) with bradycardia (-48.7 beats/min) in 21 of 31 cats was mediated by the C fibers in the right vagal cardiac nerve trunk. The efferent pathway for the bradycardia was in caudal cardiac branches of the right vagus. Neither sympathetic denervation to the heart nor atropine attenuated the hypotensive response significantly, suggesting that the depressor response results from reflex inhibition of peripheral sympathetic activity. A pressor reflex without heart rate change was observed either when the vagi were blocked or when the distribution of vagal afferents in the pericoronary nerve was considered to be small. The pressor reflex was mainly mediated by the afferent C fibers within the left cardiac sympathetic nerves. The depressor response was enhanced by sympathectomy, suggesting the sympathetic counteraction on the inhibitory vagal afferents, Similarly, an enhancement of the pressor reflex by vagal blockade was observed, indicating tonic vagal restraint on excitatory sympathetic reflexes.

Motor reflexes of stomach elicited by phenyldiguanide in the rat

1980 ◽  
Vol 58 (4) ◽  
pp. 352-359 ◽  
Author(s):  
K. S. Rao
Keyword(s):  
Motor Activity ◽  
Motor Response ◽  
Sympathetic Nerves ◽  
Vagal Afferents ◽  
Intragastric Pressure ◽  
Motor Responses ◽  
Efferent System ◽  
Efferent Pathway ◽  
Cervical Vagotomy ◽  
Stimulation Of

Intragastric pressure (IGP) as an index of gastric motor activity was used to investigate gastric motor responses elicited by phenyldiguanide (PDG) in rats under pentobarbitone anaesthesia. Phenyldiguanide injected into the atrium produced an inhibitory gastric motor response whereas an aortic injection resulted in an increase in IGP. Intracarotid injections were without effect. Atropine reduced the response to atrial PDG but not to aortic PDG. Cervical vagotomy abolished the response to both atrial and aortic PDG. Guanethidine and spinal transection abolished the response to atrial PDG only. It is concluded that PDG acts by stimulation of nonmedullated vagal afferents. The efferent pathway for PDG-evoked gastric relaxation is through sympathetic nerves and the efferent system for gastric contraction involves a noncholinergic, nonadrenergic excitatory mechanism.

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)

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.

Sympathetic neural effects on regional atrial recovery properties and cardiac rhythm

1981 ◽  
Vol 240 (4) ◽  
pp. H590-H596
Author(s):  
F. A. Kralios ◽  
C. K. Millar
Keyword(s):  
Left Atrial ◽  
Sinus Node ◽  
Stellate Ganglion ◽  
Sympathetic Nerves ◽  
Substantial Effect ◽  
Cardiac Nerve ◽  
Anesthetized Dogs ◽  
Functional Distribution ◽  
The Right ◽  
Stimulation Of

The functional distribution of the cardiac sympathetic nerves to the atria and their arrhythmiogenic effects were determined in 16 open-chest pentobarbital-anesthetized dogs. Shortening of refractory periods at four right and two left atrial sites during stimulation of the nerves was taken as a criterion of their distribution. Stimulation of right stellate ganglion, craniovagal, and right stellate cardiac nerves produced localized shortening on the right atrium, particularly at the sinus node area, and invariably induced sinus tachycardia. The recurrent cardiac nerve produced little shortening at all sites and less arrhythmiogenic effect. The left stellate ganglion and ventrolateral cardiac nerve affected only left atrial sites and induced atrioventricular junctional rhythm. The ventromedial cardiac nerve affected all sites and had no consistent arrhythmiogenic effect. The innominate nerve had no substantial effect. We concluded that the functional distribution of the cardiac sympathetic nerves is localized, and that rate, rhythm, and refractory period changes induced by stimulation of these nerves are characteristic of the area of distribution.

Reflex responses to stimulation of baroreceptors in the right subclavian artery

1964 ◽  
Vol 206 (4) ◽  
pp. 918-922 ◽  
Author(s):  
Hiromasa Okada
Keyword(s):  
Subclavian Artery ◽  
Impulse Activity ◽  
Sympathetic Nerves ◽  
Appreciable Change ◽  
Anesthetized Dogs ◽  
The Right ◽  
Carotid Arterial ◽  
Decerebrate Cats ◽  
Common Carotid Arteries ◽  
Stimulation Of

The effect of stimulation of the baroreceptors of the right subclavian artery upon the efferent impulse activity of the cardioregulatory and abdominal sympathetic nerves was investigated in decerebrate cats and anesthetized dogs. Increase in the pressure in the isolated and perfused right subclavian-carotid arterial segment diminished or abolished the impulse activity in the cardiac and abdominal sympathetic nerves. Simultaneously there was an increase of impulse activity in the cardiac vagus. No appreciable change of impulse activity in the long ciliary nerve was noticed. Impulse activity in the cardiac vagus nerve was found to be predominant during expiration both in decerebrated and anesthetized dogs with bilateral occlusion of the common carotid arteries.

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

1997 ◽  
Vol 82 (3) ◽  
pp. 765-771 ◽  
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.

Supersensitivity to l-norepinephrine of the denervated sinoatrial node

1965 ◽  
Vol 208 (2) ◽  
pp. 255-259 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd
Keyword(s):  
Vagus Nerve ◽  
Sinoatrial Node ◽  
Sinus Node ◽  
Sympathetic Nerves ◽  
Cardiac Denervation ◽  
Cervical Vagotomy ◽  
Cervical Ganglia ◽  
The Right ◽  
Cardiac Nerves ◽  
Stimulation Of

Following attempted denervation of the heart by the technic of regional neural ablation, dogs with incomplete cardiac denervation were shown to have the same supersensitivity to l-norepinephrine as dogs in which the denervation of the heart was complete. Dogs with chronic bilateral stellate ganglionectomy or those pretreated with reserpine had cardiac acceleration in response to the administration of tyramine or to stimulation of the stellate cardiac nerves, but did not demonstrate supersensitivity to l-norepinephrine. No supersensitivity was seen in dogs with chronic bilateral cervical vagotomy. Excision of the right stellate and caudal cervical ganglia and the immediately adjacent right vagus nerve resulted in supersensitivity to l-norepinephrine. In these animals cardiac acceleration resulted from stimulation of the left stellate cardiac nerves or from the administration of tyramine. The supersensitivity was lost after excision of the sinoatrial node. It is concluded that one can uniquely denervate the sinus node and that dogs so treated will develop supersensitivity to l-norepinephrine despite the presence of functional sympathetic nerves to the rest of the heart.

Stimulation of vagal afferents inhibits locomotion in mesencephalic cats

1993 ◽  
Vol 74 (1) ◽  
pp. 103-110 ◽  
Author(s):  
J. G. Pickar ◽  
J. M. Hill ◽  
M. P. Kaufman
Keyword(s):  
Intravenous Injection ◽  
Left Atrial ◽  
Onset Time ◽  
Vagal Afferents ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
C Fibers ◽  
Cervical Vagotomy ◽  
Reflex Arc ◽  
Stimulation Of

Using electrical stimulation of the mesencephalic locomotor region, we made decerebrate unanesthetized cats walk on a treadmill. The locomotion induced by stimulation of this midbrain area was assessed before and during activation of vagal afferents by either intravenous injection of phenylbiguanide or inflation of a balloon placed in the left atrium. Inflation of a balloon, which increased left atrial pressure by 7–25 mmHg, abolished locomotion in 9 of 10 cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by balloon inflation in each of two cats tested. Intravenous phenylbiguanide (50 or 100 micrograms/kg) or serotonin (40 micrograms/kg) injections abolished or attenuated walking induced by midbrain stimulation in 11 of 13 cats tested. In addition, intravenous phenylbiguanide injections abolished or attenuated locomotion with a shorter onset time than did systemic injections of this substance in five of six cats tested. Bilateral cervical vagotomy prevented the abolition of locomotion by phenylbiguanide injection in each of five cats tested. We conclude that locomotion can be prevented by a viscerosomatic reflex arising from the lungs and heart. The afferent arm of this reflex arc is the vagus nerve. Afferents such as slowly and rapidly adapting pulmonary stretch receptors, atrial receptors, and lung C-fibers may have had a role in preventing locomotion during the increase in left atrial pressure in our experiments. On the other hand, pulmonary C-fibers had a crucial role in preventing locomotion during intravenous injection of phenyl-biguanide. We speculate that this viscerosomatic reflex may help to explain in part the intolerance for exercise displayed by patients with congestive heart failure.

Cooling the pulmonary blood in dogs alters activity of pulmonary vagal afferents

1993 ◽  
Vol 74 (1) ◽  
pp. 24-30 ◽  
Author(s):  
G. G. Giesbrecht ◽  
T. E. Pisarri ◽  
J. C. Coleridge ◽  
H. M. Coleridge
Keyword(s):  
Pressure Effects ◽  
Vagal Afferents ◽  
High Threshold ◽  
Control Frequency ◽  
C Fibers ◽  
Cold Blood ◽  
Right Pulmonary Artery ◽  
Anesthetized Dogs ◽  
Exercise Induced ◽  
The Right

In open-chest anesthetized dogs with left and right lungs ventilated separately, we recorded changes in firing of right lung vagal receptors when 1.25 ml/kg cold (5 degrees C, 20 degrees C) blood were injected into the nonperfused right pulmonary artery. With the right lung inflated at constant pressure, effects of cold blood on individual pulmonary stretch receptors (PSRs) were frequency dependent, with discharge increasing or remaining unchanged if control frequency was low and decreasing if it was high. Consequently average PSR discharge was unchanged by cold blood when airway pressure was maintained at 5 cmH2O, but it decreased at pressures of 10 and 15 cmH2O. Cold blood stimulated rapidly adapting receptors (RARs) at all three pressures. Injection of blood at 37 degrees C had no effect. We conclude that changes in PSR activity account for the tachypnea induced by pulmonary arterial injection of cold blood (G. G. Giesbrecht and M. Younes. J. Appl. Physiol. 69: 1435–1441, 1990). With the right lung phasically ventilated, cold blood decreased PSR discharge in inflation, caused high-threshold PSRs to fire in deflation, and stimulated RARs. Pulmonary C-fibers were unaffected by cold blood. We suggest that PSRs and RARs initiate respiratory changes during hypothermia or exercise-induced asthma.

Cigarette smoke in lungs evokes reflex increase in tracheal submucosal gland secretion in dogs

1991 ◽  
Vol 71 (3) ◽  
pp. 900-909 ◽  
Author(s):  
H. D. Schultz ◽  
B. Davis ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Cigarette Smoke ◽  
Lung Compliance ◽  
Vagal Afferents ◽  
Gland Secretion ◽  
Submucosal Gland ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Lower Trachea ◽  
Stimulation Of

Stimulation of pulmonary C-fibers (PCs) by capsaicin and of rapidly adapting receptors (RARs) by reduced lung compliance reflexly increases airway submucosal gland secretion in dogs. Because both PCs and RARs are stimulated by cigarette smoke (nicotine being the primary stimulus), we performed experiments in anesthetized open-chest artificially ventilated dogs (with aortic nerves cut) to determine whether cigarette smoke reflexly stimulates airway secretion. We measured submucosal gland secretion by counting the hillocks in a 1.2-cm2 field of tracheal epithelium coated with tantalum dust. Secretion was stimulated by delivery of 40–320 ml smoke from high-nicotine cigarettes to the lower trachea, secretion rate increasing from 7.4 +/- 1.3 to 48.1 +/- 5.1 hillocks.cm-2.min-1. Results of cutting the pulmonary vagal branches or carotid sinus nerves or both indicated that the secretory response was initiated by stimulation of lower respiratory vagal afferents and augmented several seconds later by stimulation of carotid chemoreceptors. Results of cooling the cervical vagus nerves to 7 and 0 degrees C indicated that most of the vagally mediated increase in secretion was due to stimulation of afferent lung C-fibers.

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