scholarly journals STUDIES WITH THE ELECTROCARDIOGRAPH ON THE ACTION OF THE VAGUS NERVE ON THE HUMAN HEART

1912 ◽  
Vol 15 (1) ◽  
pp. 14-48 ◽  
Author(s):  
Canby Robinson ◽  
George Draper

The electrocardiographic records taken during vagus stimulation by pressure from children suffering with chronic heart disease have shown that the stimulation of the vagi in these cases is strikingly effectual. In some of the cases, a definite difference was demonstrated between the action of the right and left vagi. The control of the rate of the heart-beat seemed to predominate usually in the right vagus nerve, while the control of stimulus conduction from auricles to ventricles apparently predominated usually in the left vagus. This difference in the two nerves probably exists on account of the difference in their anatomical distribution, the right vagus going especially to that part of the heart which controls the rate of contraction, the sinus node above the right auricle, and the left vagus going especially to that part in which the conducting mechanism is found. Each nerve, however, has to a lesser degree the function which predominates in the other. The whole heart seems to respond, as a rule, more promptly to right than to left vagus pressure, and fairly constant differences have been seen in the effects which stimulation of each nerve has on the various waves of the electrocardiograms. The stimulation of each vagus may influence directly the contractions of the ventricles, causing great diminution in their force. Right vagus stimulation was followed at times by a complete dissociation of auricles and ventricles. The auricular rhythm was slowed sufficiently at this time to allow the ventricles, whose inherent rhythmicity is apparently unaffected by right vagus stimulation, to take up their own independent rhythm. The heightened ventricular rhythmicity in these cases allowed this to take place after only moderate slowing of the auricles. The independent ventricular rhythm was sometimes established in the region of the node of Tawara, for no disturbance of the ventricular portion of the electrocardiogram occurred. At another time, some other point in the ventricles inaugurated the stimuli of the independent ventricular contractions and an abnormal electrocardiogram resulted. The resemblance of our curves, showing dissociation, to those obtained during right vagus and left accelerator stimulation in dogs is definite. That analogy, the clinical picture, and the form of the electrocardiograms of these cases have led us to the belief that an important feature in the pathological physiology of these cases is hypertonus of the cardiac accelerator nerves. This factor, as a cause of symptoms and as a hindrance to the establishment of cardiac rest, may prove of great importance, against which a new form of cardiac therapeutics must be directed.

1913 ◽  
Vol 18 (6) ◽  
pp. 704-714
Author(s):  
G. Canby Robinson

The tumultuous auricular activity which follows faradization of the auricles of mammals and which has been variously described, could be distinctly seen to consist almost constantly in our experiments on dogs of true fibrillatory movements of the separate muscle fibers coëxisting with a rapid auricular tachycardia. During peripheral stimulation of the right vagus nerve the true fibrillation alone existed, the tachycardia being inhibited. A comparison of the electrocardiograms from dogs with this abnormal auricular activity with those from patients with the type of cardiac arhythmia which has been attributed to auricular fibrillation, and from patients with so called auricular flutter, indicates that the auricular activity in patients with either of these conditions differs somewhat from that usually seen in the faradized auricles of the dog in our experiments. The auricular activity of the cases of cardiac arhythmia is apparently true fibrillation, similar to that seen in the faradized auricles of the dog during right vagus stimulation. The electrocardiograms from cases of so called auricular flutter usually give no evidence of auricular fibrillation, and the auricular activity seems to consist of tachycardia alone. Fibrillation may apparently coëxist with the tachycardia in some cases, when the auricular activity seems to resemble closely that usually seen in the dog after auricular faradization. During peripheral stimulation of the left vagus nerve, the electrocardiograms obtained after auricular faradization show changes which render them more nearly similar to those obtained from patients with auricular flutter. The facts that the auricular activity of the faradized auricles of the dog may apparently pass spontaneously into that closely resembling auricular flutter in man, that it may be changed into true fibrillation by right vagus stimulation, and that the abnormal auricular activity in man passes from a state of flutter to that of fibrillation in a similar manner, may be taken as evidence for the belief that auricular fibrillation and auricular flutter in man are closely allied cardiac disorders.


1913 ◽  
Vol 17 (4) ◽  
pp. 429-443 ◽  
Author(s):  
G. Canby Robinson

An abnormal auricular activity is produced by faradization of the right auricle of the dog, which frequently becomes established and continues for varying periods of time after faradization is discontinued. This auricular activity consists of a rapid auricular tachycardia coexisting with true auricular fibrillation. In some dogs the auricles are thrown into this abnormal activity more readily by faradization after the vagi have been cut than before. Cutting the nerves has little or no effect on the abnormal auricular activity, but the ventricular rate may be much increased if the vagi are cut after the abnormal auricular activity has been established, apparently because of an improvement in the auriculoventricular conductivity. Stimulation of the right vagus nerve changes the character of the activity of the faradized auricles by inhibiting the auricular tachycardia while the fibrillation is uninfluenced. Stimulation of the left vagus nerve has little or no apparent inhibitory effect on the auricular tachycardia, but has possibly an inhibitory effect on the auricular fibrillation. Vagus stimulation increases the susceptibility of the auricles to faradization. The abnormal activity set up by faradization may be established in hearts otherwise refractory by vagus stimulation of short duration following the faradization. Vagus stimulation usually holds the auricles in the abnormal activity set up by faradization as long as it is continued in hearts in which, without vagus stimulation, the sequential beat always returns as soon as faradization is stopped. The right vagus is more effectual in this respect than the left. In some hearts vagus stimulation alone is capable of initiating the same abnormal auricular activity which is caused by auricular faradization. The normal sequential beat is often restored by vagus stimulation. It replaces the abnormal auricular activity not during, but a few seconds after, the termination of vagus stimulation. Left vagus stimulation is somewhat more effectual in producing this result than right vagus stimulation.


1911 ◽  
Vol 14 (3) ◽  
pp. 217-234 ◽  
Author(s):  
G. Canby Robinson ◽  
George Draper

In hearts showing auricular fibrillation mechanical stimulation of the right vagus nerve causes, as a rule, marked slowing or stoppage of ventricular rhythm, without producing any appreciable effect in the electrocardiographic record of the auricular fibrillation. The ventricular pauses are apparently due to the blocking of stimuli from the auricles. The force of ventricular systole is distinctly weakened for several beats after vagus stimulation, and ectopic ventricular systoles have been seen in several instances, apparently the result of the vagus action. There may, in some cases, be lowered excitability of the ventricles, while no constant change is seen in the size of the electrical complexes representing ventricular systole.


2000 ◽  
Vol 89 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Robert L. Coon ◽  
Patrick J. Mueller ◽  
Philip S. Clifford

The canine cervical trachea has been used for numerous studies regarding the neural control of tracheal smooth muscle. The purpose of the present study was to determine whether there is lateral dominance by either the left or right vagal innervation of the canine cervical trachea. In anesthetized dogs, pressure in the cuff of the endotracheal tube was used as an index of smooth muscle tone in the trachea. After establishment of tracheal tone, as indicated by increased cuff pressure, either the right or left vagus nerve was sectioned followed by section of the contralateral vagus. Sectioning the right vagus first resulted in total loss of tone in the cervical trachea, whereas sectioning the left vagus first produced either a partial or no decrease in tracheal tone. After bilateral section of the vagi, cuff pressure was recorded during electrical stimulation of the rostral end of the right or left vagus. At the maximum current strength used, stimulation of the left vagus produced tracheal constriction that averaged 28.5% of the response to stimulation of the right vagus (9.0 ± 1.8 and 31.6 ± 2.5 mmHg, respectively). In conclusion, the musculature of cervical trachea in the dog appears to be predominantly controlled by vagal efferents in the right vagus nerve.


1916 ◽  
Vol 24 (5) ◽  
pp. 605-619 ◽  
Author(s):  
G. Canby Robinson

The experiments that have been reported indicate that stimulation of either the right vagus or the left vagus nerve is equally effectual in blocking impulses from the auricles to the ventricles when auricular fibrillation is present. Stimulation of the left vagus nerve is as effectual in blocking impulses from the normally beating auricles as from the auricles when in a state of fibrillation, and the type of auricular activity has apparently no influence on the effect which stimulation of the left vagus has on auriculoventricular conduction.


1989 ◽  
Vol 256 (5) ◽  
pp. H1295-H1302
Author(s):  
S. A. Lang ◽  
M. N. Levy

We determined the effects of vagus nerve stimulation on cardiac cycle length and on ventricular contraction and relaxation in 18 chickens anesthetized with pentobarbital. Right vagus stimulation at a constant frequency of 35 Hz prolonged cycle length by 190%, whereas left vagus stimulation at the same frequency increased cycle length by 136%. When one burst of stimuli was delivered to the right vagus nerve each cardiac cycle, but the timing of the stimuli was changed within the cardiac cycle, the response of the avian pacemaker cells varied substantially with the timing of the stimuli. Right and left vagus stimulation at a constant frequency of 20 Hz depressed ventricular contraction by 62 +/- 6 and 52 +/- 6%, respectively, and depressed ventricular relaxation by 56 +/- 7 and 53 +/- 7%, respectively. These results indicate that in the chicken the chronotropic effects of right vagus stimulation are greater than those of left vagus stimulation, whereas right and left vagus stimulation are approximately equipotent on ventricular contraction and relaxation.


1965 ◽  
Vol 208 (2) ◽  
pp. 255-259 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd

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.


1912 ◽  
Vol 16 (6) ◽  
pp. 732-757 ◽  
Author(s):  
Alfred E. Cohn

It may be concluded from the results obtained in these experiments : 1. That stimulation of the right vagus nerve in the dog usually causes arrest of all the chambers of the heart. 2. That stimulation of the left vagus nerve exerts a moderate negative chronotropic effect on the auricles. 3. That stimulation of the left vagus nerve has a profound effect on the conduction of impulses over the auriculoventricular system. 4. That the degree of effect exercised on the auriculoventricular system by stimulation of the left vagus nerve varies. In some dogs conduction is depressed to an extent which causes only a delay in the conduction of impulses from auricles to ventricles (P-R time) ; in other dogs the conduction is depressed to a degree which results in incomplete heart-block; while in still other dogs conduction is so depressed that although the auricles continue to contract, no impulses pass from them to the ventricles. 5. That when stimulation of either the right or left vagus nerve causes asystole of nomotopic ventricular contractions, ectopic ventricular contractions may occur. 6. That the time which elapses before ectopic ventricular contractions occur depends upon the irritability of the ventricular muscle, and this may vary in different dogs. 7. That stimulation of the left vagus nerve may rarely cause sino-auricular block. Possibly stimulation of the right nerve may also produce this effect. 8. That there is consequently usually a great qualitative difference in the action of the two vagus nerves on the heart of the dog.


2020 ◽  
Vol 73 (2) ◽  
pp. 224-228
Author(s):  
Orysia O. Bandrivska ◽  
Vitalij M. Mykhailiuk ◽  
Iryna A. Mykhailiuk ◽  
Natalia V. Malko

The aim: Find out the nature of the changes sensitivity of the heart to the cholinergic influences the development of diabetes depending on gender. Materials and methods: In experiments on adult male and female rats, type 1 diabetes by momentary introduction of streptozotocin at a dose of 60 mg/ kg into the peritoneal cavity was modeled. Animals were examined after 15, 30, 60 and 90 days after introduction of streptozotocin. We studied the sensitivity of cholinoreceptors of sinus node by the intensity of bradycardia with intravenous injection of acetylcholine and electrical stimulation of the peripheral segment of the right vagus nerve. Results: It was established that the intensity of the negative chronotropic effect of heart of males by electric stimulation of the vagus nerve, which depends on the reserves of acetylcholine in the presynaptic section and sensitivity of postsynaptic cholinoreceptors, increased gradually and after 90 days prevailed the output value in 2.2 times. This occurred at the background of a slight (10 %) decrease in response to exogenous acetylcholine that reflected the decrease in sensitivity of cholinoreceptors. In females the maximum increase (in 4.4 times) of the intensity of the negative chronotropic effect of vagus nerve stimulation was observed after 30 days from the start of the experiment. After 90 days, this indicator prevailed the controlled one in 3.3 times, which occurred at the background of heart response decreasing to exogenous acetylcholine (in 1.7 times). Conclusions: Obtained results suggest a more significant change in state of cholinoceptor system of myocardium of females compared with males in the dynamics of development of streptozotocin-induced diabetes.


EP Europace ◽  
2021 ◽  
Vol 23 (Supplement_3) ◽  
Author(s):  
A Scridon ◽  
VB Halatiu ◽  
AI Balan ◽  
DA Cozac ◽  
GV Moldovan ◽  
...  

Abstract Funding Acknowledgements Type of funding sources: Public grant(s) – National budget only. Main funding source(s): This work was supported by a grant of the Romanian Ministry of Education and Research, CNCS - UEFISCDI Background The autonomic control of the pacemaker current, If, and the molecular mechanisms underlying parasympathetic If modulation are well understood. Conversely, the effects of chronic If blockade on the parasympathetic nervous system and on the heart rate (HR) response to acute parasympathetic changes are still largely unknown. Such interactions could significantly influence the course of patients undergoing chronic therapy with the If blocker ivabradine. Purpose We aimed to assess the effects of long-term If blockade using ivabradine on cardiac autonomic modulation and on the cardiovascular response to acute in vivo and in vitro parasympathetic stimulation. Methods Radiotelemetry ECG transmitters were implanted in 6 Control and 10 ivabradine-treated male Wistar rats (IVA; 3 weeks, 10 mg/kg/day); sympathetic and parasympathetic heart rate variability parameters were assessed. At the end of the study, the right atrium was removed and right atrial HCN(1-4) RNA expression levels were analyzed. The HR and systolic blood pressure (SBP) responses to in vivo electrical stimulation of the right vagus nerve (2–20 Hz) and the spontaneous sinus node discharge rate (SNDR) response to in vitro cholinergic receptors stimulation using carbamylcholine (10-9–10-6 mol/L) were assessed in 6 additional Control and 10 IVA rats. Results At the end of the study, mean 24-h HR was significantly lower in the IVA compared with the Control rats (301.3 ± 7.5 bpm vs. 341.5 ± 8.3 bpm; p< 0.01). Ivabradine administration led to a significant increase in vagal tone and shifted the sympatho-vagal balance towards vagal dominance (awake, asleep, and over 24-h; all p< 0.05). In the Control rats, in vivo vagus nerve stimulation induced a progressive decrease in both the SBP (p = 0.0001) and the HR (p< 0.0001). Meanwhile, in the IVA rats, vagal stimulation had no effect on the HR (p = 0.16) and induced a significantly lower drop in SBP (p< 0.05). Ivabradine-treated rats also presented a significantly lower SNDR drop in response to carbamylcholine (p< 0.01) and significantly higher HCN4 expression (p = 0.02). Conclusion Long-term If blockade using ivabradine caused a significant increase in vagal tone and shifted the autonomic balance towards vagal dominance in rats. Given the highly proarrhythmic effects of vagal activation at the atrial level, these findings could provide an explanation for the increased risk of atrial fibrillation associated with ivabradine use in clinical trials. In addition, ivabradine reduced the HR response to direct muscarinic receptors stimulation, canceled the cardioinhibitory response and blunted the hemodynamic response to in vivo vagal stimulation, and led to significant sinus node HCN4 up-regulation. These data suggest that ivabradine-induced HCN4 and the consequent If up-regulation could render the sinus node less sensitive to acute vagal inputs and could thus protect against excessive bradycardia induced by acute vagal activation.


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