SITES OF VAGAL ACTION IN ADRENALINE-INDUCED CARDIAC ARRHYTHMIAS

1962 ◽  
Vol 40 (1) ◽  
pp. 1655-1661
Author(s):  
Peter E. Dresel
Keyword(s):  
Ventricular Arrhythmia ◽  
Cardiac Arrhythmias ◽  
Sinus Bradycardia ◽  
Threshold Dose ◽  
Pacemaker Activity ◽  
Vagus Nerves ◽  
Atrial Rate ◽  
Anesthetized Dogs ◽  
Complete Atrioventricular

Intact vagus nerves are necessary for consistent induction of ventricular arrhythmia by adrenaline in barbiturate-anesthetized dogs although sinus bradycardia does not necessarily precede ventricular pacemaker activity. We have found that the threshold dose of adrenaline is not affected by maintaining the atrial rate electrically. In driven hearts, arrhythmia is preceded by partial or complete atrioventricular (AV) nodal block. AV nodal block is also observed without emergence of the ventricular pacemaker. AV nodal block during "nodal rhythm" induced by adrenaline in normal hearts has been demonstrated. It is concluded that although ventricular slowing always precedes ventricular arrhythmia in these preparations, the action of the vagi on nodal conduction is sufficient to allow emergence of the ventricular pacemaker both in the presence and the absence of maintained atrial rates.

SITES OF VAGAL ACTION IN ADRENALINE-INDUCED CARDIAC ARRHYTHMIAS

1962 ◽  
Vol 40 (12) ◽  
pp. 1655-1661 ◽  
Author(s):  
Peter E. Dresel
Keyword(s):  
Ventricular Arrhythmia ◽  
Cardiac Arrhythmias ◽  
Sinus Bradycardia ◽  
Threshold Dose ◽  
Pacemaker Activity ◽  
Vagus Nerves ◽  
Atrial Rate ◽  
Anesthetized Dogs ◽  
Complete Atrioventricular

Intact vagus nerves are necessary for consistent induction of ventricular arrhythmia by adrenaline in barbiturate-anesthetized dogs although sinus bradycardia does not necessarily precede ventricular pacemaker activity. We have found that the threshold dose of adrenaline is not affected by maintaining the atrial rate electrically. In driven hearts, arrhythmia is preceded by partial or complete atrioventricular (AV) nodal block. AV nodal block is also observed without emergence of the ventricular pacemaker. AV nodal block during "nodal rhythm" induced by adrenaline in normal hearts has been demonstrated. It is concluded that although ventricular slowing always precedes ventricular arrhythmia in these preparations, the action of the vagi on nodal conduction is sufficient to allow emergence of the ventricular pacemaker both in the presence and the absence of maintained atrial rates.

The effect of destruction of the bundle of His or the atrioventricular node on cyclopropane–adrenaline cardiac arrhythmias

1970 ◽  
Vol 48 (4) ◽  
pp. 207-215 ◽  
Author(s):  
Betty I. Sasyniuk ◽  
Peter E. Dresel
Keyword(s):  
Coronary Artery ◽  
Cardiac Arrhythmias ◽  
Atrioventricular Node ◽  
Circumflex Coronary Artery ◽  
Selective Destruction ◽  
Anesthetized Dogs ◽  
Bundle Of His

Destruction of the bundle of His abolished bigeminal rhythms produced by adrenaline in thiopentone–cyclopropane anesthetized dogs. Bigeminal rhythms were still elicited, however, after selective destruction of the A–V node. Destruction of the bundle of His did not prevent multifocal arrhythmias but did increase the dose of adrenaline required to induce them. Multifocal arrhythmias produced after destruction of the bundle of His were abolished by injections of acetylcholine into the left anterior descending, but not the circumflex coronary artery, results opposite to those obtained in normal hearts.

Atrial-specific drug AVE0118 is free of torsades de pointes in anesthetized dogs with chronic complete atrioventricular block

Heart Rhythm ◽  
2006 ◽  
Vol 3 (11) ◽  
pp. 1339-1345 ◽  
Author(s):  
Avram Oros ◽  
Paul G.A. Volders ◽  
Jet D.M. Beekman ◽  
Theo van der Nagel ◽  
Marc A. Vos
Keyword(s):  
Atrioventricular Block ◽  
Torsades De Pointes ◽  
Specific Drug ◽  
Complete Atrioventricular Block ◽  
Anesthetized Dogs ◽  
Complete Atrioventricular

Limited hypertensive effect of infusion of angiotensin

1965 ◽  
Vol 209 (2) ◽  
pp. 264-268 ◽  
Author(s):  
Michael D. Day ◽  
James W. McCubbin ◽  
Irvine H. Page
Keyword(s):  
Arterial Pressure ◽  
Renal Hypertension ◽  
Initial Pressure ◽  
Pressure Level ◽  
Cardiovascular Reflexes ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
Experimental Renal Hypertension ◽  
Maximal Pressure ◽  
Renal Artery Constriction

Though single injections of angiotensin cause extreme rise in arterial pressure, infusion fails to elevate pressure to the degree usually found in experimental renal hypertension. The maximal pressure level obtainable by infusing angiotensin into anesthetized dogs was approximately the same in different dogs and was independent of the initial pressure. The vagus nerves did not importantly influence the "ceiling" response but if arterial pressure was then elevated by carotid occlusion the ceiling was raised. The combination of renal artery constriction and infusion of angiotensin failed to give a higher ceiling than angiotensin alone. In dogs with chronic renal hypertension the ceiling was higher than in normal dogs, presumably because of an upward shift in the range of response of cardiovascular reflexes. The results support the view that compensatory cardiovascular reflexes and tachyphylaxis to large amounts of infused angiotensin suppress the response and that these factors are much less effective in limiting response to quick injection.

Reflex bronchial vasodilation in dogs evoked by injection of a small volume of water into a bronchus

1993 ◽  
Vol 75 (5) ◽  
pp. 2195-2202 ◽  
Author(s):  
T. E. Pisarri ◽  
H. M. Coleridge ◽  
J. C. Coleridge
Keyword(s):  
Blood Flow ◽  
Mucosal Blood Flow ◽  
Vagus Nerves ◽  
C Fibers ◽  
Autonomic Pathways ◽  
Lobar Bronchus ◽  
Anesthetized Dogs ◽  
Pharmacological Blockade ◽  
Airway Defense ◽  
Response To Water

Injection of water into a lobar bronchus stimulates airway C-fibers and rapidly adapting receptors and evokes airway defense reflexes. To determine whether this stimulus also evokes a reflex increase in bronchial blood flow (Qbr), we injected 1–2 ml of water into a lobar bronchus in anesthetized dogs. Injection decreased arterial pressure but increased Qbr from 9 +/- 1 to 21 +/- 3 ml/min. The increase had a latency of 6–8 s and reached a peak after approximately 20 s; Qbr returned to control after 60–90 s. Airway mucosal blood flow, measured by colored microspheres, increased in proportion to Qbr. In contrast, flow in an adjacent intercostal artery that did not supply the airway decreased slightly. Injection of isosmotic saline had little effect. In 13 of 16 dogs, the water-induced increase in Qbr was abolished by cutting or cooling the cervical vagus nerves and hence was entirely dependent on centrally mediated vagal pathways. When the vagus nerves were intact, about one-third of the vasodilator response remained after pharmacological blockade of muscarinic and adrenergic receptors. We conclude that in dogs the defense response to water in the lower airways includes a large increase in Qbr that is partly due to activation of nonadrenergic noncholinergic autonomic pathways.

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.

Expiratory threshold load under extracorporeal circulation: effects of vagal afferents

1983 ◽  
Vol 55 (2) ◽  
pp. 307-315 ◽  
Author(s):  
Y. Jammes ◽  
P. T. Bye ◽  
R. L. Pardy ◽  
C. Katsardis ◽  
S. Esau ◽  
...  
Keyword(s):  
Mechanical Vibration ◽  
Muscle Spindles ◽  
Vagal Afferents ◽  
Abdominal Muscles ◽  
Vagus Nerves ◽  
Linea Alba ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Proprioceptive Afferents

Nine anesthetized dogs breathed against an expiratory threshold load (ETL) applied by switching the expiratory circuit into a column of H2O to a depth of 20-30 cm. Arterial blood gas tensions were maintained in the normal range by placing the dogs under arteriovenous bypass to avoid any uncontrolled chemostimulation. There was an increase in integrated electromyogram activity of the diaphragm with the ETL. This was rarely observed after cold block of the vagus nerves which also reduced the evoked expiratory activity. The ventilatory response to hypercapnia was greatly depressed under loaded breathing whether vagal afferents were intact or blocked by cold. Both inspiratory drive and ventilatory timing were affected, suggesting that the central integration of chemosensitive afferents was altered. Proof of supraspinal projections of proprioceptive inputs from abdominal muscles was provided by the demonstration of changes in ventilatory timing during selective activation of muscle spindles in abdominal muscles by high-frequency mechanical vibration applied to the linea alba. Thus these observations suggest that during ETL breathing, a possible interaction exists between chemoreflex drive and proprioceptive afferents.

Hypoxemia reflexly increases secretion from tracheal submucosal glands in dogs

1982 ◽  
Vol 52 (6) ◽  
pp. 1416-1419 ◽  
Author(s):  
B. Davis ◽  
R. Chinn ◽  
J. Gold ◽  
D. Popovac ◽  
J. G. Widdicombe ◽  
...  
Keyword(s):  
Carotid Body ◽  
Carotid Sinus ◽  
Gland Secretion ◽  
Submucosal Gland ◽  
Vagus Nerves ◽  
Epithelial Surface ◽  
O2 Concentration ◽  
Submucosal Glands ◽  
Lower Trachea ◽  
Anesthetized Dogs

We anesthetized dogs, ventilated their lungs via the lower trachea, and exposed the epithelial surface of the upper trachea and coated it with powdered tantalum. Secretions from submucosal gland ducts formed elevations (hillocks) in the tantalum layer; we counted the number of hillocks that appeared in a 1.2-cm2 field. In 12 dogs, during normoxemia, 12 +/- 2 hillocks/cm2 formed in 90 s; during severe hypoxemia [fractional inspired O2 concentration (FIO2) = 0.05], 40 +/- 4 hillocks/cm2 formed in 90 s. Injections of sodium cyanide (25–75 micrograms) into the arterial supply to the carotid body also stimulated tracheal submucosal gland secretion. Secretory response to hypoxemia was suppressed by 1) section of both carotid sinus body nerves in six dogs and 2) section of both superior laryngeal nerves and vagus nerves in six other dogs. During mild hypoxemia (FIO2 = 0.10 or 0.15) tracheal submucosal gland secretion still increased. We conclude that hypoxemia increases secretion from submucosal glands in canine trachea by a carotid body chemoreflex.

Neonatal Tachyarrhythmias

2000 ◽  
Vol 19 (7) ◽  
pp. 45-51
Author(s):  
Margaret Watson
Keyword(s):  
Atrial Flutter ◽  
Supraventricular Tachycardia ◽  
Cardiac Arrhythmias ◽  
Heart Block ◽  
Ventricular Arrhythmias ◽  
Sinus Bradycardia

CARDIAC ARRHYTHMIAS CAN BE found in the fetus and the neonate. Arrhythmias that are seen in the neonate include sinus bradycardia and tachycardia, premature atrial and ventricular contractions, supraventricular tachycardia, atrial flutter, ventricular arrhythmias, and heart block. Although infants with structural or functional anomalies can have arrhythmias, many arrhythmias result from noncardiac causes, such as hypoxemia and acidosis.1

Heart rate and rhythm and intracranial pressure

1976 ◽  
Vol 230 (6) ◽  
pp. 1695-1700 ◽  
Author(s):  
JA Krasney ◽  
RC Koehler
Keyword(s):  
Heart Rate ◽  
Intracranial Pressure ◽  
Pressor Response ◽  
Sinus Bradycardia ◽  
Autonomic Nerves ◽  
Balloon Inflation ◽  
Cardiac Dysrhythmias ◽  
Cardiac Slowing ◽  
Intracranial Lesions ◽  
Anesthetized Dogs

Cardiac slowing during elevated intracranial pressure (ICP) could be due to direct activation of central nervous system (CNS) centers or it may be secondary to baroreceptor reflexes activated by the associated pressor response. In five pentobarbital-anesthetized dogs when ICP was raised to 50 mmHg the heart rate decreased 34.4 beats/min (+/-4.8 SE). This cardiac slowing occurred when ICP was elevated after sinoaortic denervation (-24 +/- 4.43 beats/min) and also during elevated ICP when changes in arterial pressure were prevented (-32.3 +/- 4.25 beats/min). These results indicate that the cardiac slowing is largely of CNS origin. In dogs given morphine with pentobarbital to achieve slower heart rates, raising ICP to 50 mmHg by left-sided intracranial balloon inflation led to cardiac dysrhythmias in 9 of 12 dogs. By contrast, raising ICP to 50 mmHg by right-sided intracranial balloon inflation only produced progressive sinus bradycardia. These responses were related to a combined enhancement of vagal and sympathetic activity. Differences observed between right- and left-sides balloon inflation may be partly related to asymmetrical engagement of the cardiac autonomic nerves. The results suggest that left-sided intracranial lesions are more likely to produce cardiac dysrhythmias.

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