Efferent Vagal Stimulation Research Articles

Substance P fails to mimic vagally mediated nonadrenergic bronchodilation

The ability of substance P to mimic vagally mediated nonadrenergic bronchodilation was assessed in vivo in anesthetized, paralyzed, artifically ventilated cats. Infusion of the peptide at a rate of 10 μg kg −1 min −1 for 10 minutes did not attenuate the increase in pulmonary resistance evoked by efferent vagal stimulation. Similarly, when administered as an aerosol (1–15 breaths of a 100 μg ml −1 aqueous solution) or by bolus intravenous injection, substance P failed to reverse the increase in pulmonary resistance maintained by a continuous intravenous infusion of 5-hydroxytryptamine. These results indicate that substance P is unlikely to be the neurotransmitter responsible for mediating nonadrenergic inhibitory responses in feline airways.

Modulation of esophageal peristalsis by vagal efferent stimulation in opossum.

Experiments were performed on anesthetized opossums to study the influence of vagal efferent stimulation on peristalsis in the esophageal smooth muscle using various stimulus parameters. Current intensity, pulse duration, frequency, and train duration were varied systematically. Electrical and mechanical activities were recorded simultaneously at 5, 3, and 1 cm above the lower esophageal sphincter (LES). Vagal efferent stimulation produced a spike burst and contraction with a latency after the termination of the stimulus. This latency varied at different sites with the same stimulus parameters. For example, a stimulus of 5 mA, 0.5 ms, 10 Hz, and 1-s train produced latencies for the electrical response of 1.48 +/- 0.04, 2.2 +/- 0.12, and 3.5 +/- 0.09 s (+/- SEM) at 5, 3, and 1 cm above LES, respectively. The differences in latency were statistically significant (P less than 0.01). The latency of response at any one site also changed with different stimulus parameters; e.g. at 1 cm above LES, the latency of electrical response at 10 Hz was 3.5 +/- 0.09 s, but at 20 Hz the latency was 2.01 +/- 0.06 s when current intensity, pulse, and train duration remained at 5 mA, 0.5 ms, and 1 s. This decrease in latency with increasing frequency was statistically significant (P less than 0.01). By changing stimulus parameters, antiperistalsis or peristalsis with different speeds of propagation could be induced. Antiperistalsis or simultaneous responses occurred near threshold stimulus parameters. Suprathreshold stimuli produced peristaltic responses. Speed of peristalsis in the distal esophagus was 1.82 +/- 0.08 cm/s with swallowing, which was not different from 1.98 +/- 0.14 cm/s (P greater than 0.05) with vagal stimulation of 5 mA, 0.5 ms, 10 Hz, and 1-s train. These studies suggest that: (a) peristalsis in the smooth muscle part of the esophagus can be explained entirely on the basis of peripheral mechanisms, and (b) the central nervous system may modulate the occurrence, polarity, and speed of propagation by modifying the intensity and frequency of vagal activation.

Suppression of the depressor cardiac reflex during coronary occlusion by lidocaine--evidence for a central nervous site of action.

The effect of lidocaine (0.35 and 0.7 mg/kg/min i.v.) on reflex cardiovascular depression was studied during coronary occlusion in 10 chloralose-anesthetized cats. Twenty to 60 s occlusion of the left anterior descending coronary artery decreased heart rate, efferent cardiac sympathetic nerve activity and blood pressure by 33.8 ± 8.8%, 56.1 ± 31.8% and 48.4 ± 13.1% of control values, respectively. During infusion of 0.35 (0.7) mg/kg/min lidocaine the heart rate was decreased by 17.6±6.1% (10.2 ±6.9), the sympathetic activity by 46.2 ± 25.5% (30.2 ± 13.4) and blood pressure by 44.7 ± 13.6% (36.4 ± 16.6) compared to controls. The same reflex was elicited in 12 cats by afferent stimulation of cardiac vagal nerve branches, and the bradycardia and decrease of blood pressure were also inhibited by lidocaine. It is concluded, that the suppression of the reflex is due to a central nervous effect of lidocaine. A possible anticholinergic effect of the drug seems to play no major role, since the bradycardia during efferent vagal stimulation (eight animals) was not affected by 0.35 mg/kg/min lidocaine.

Relation between electrical and mechanical activity in esophageal smooth muscle

Experiments were performed in anesthetized opossums. Electrical and mechanical activity was recorded simultaneously from the esophageal body at 5, 3, and 1 cm above the lower esophageal sphincter (LES). Esophageal responses were evoked by electrical stimulation of vagal efferents or by induced swallowing. Electrical and mechanical activity was associated in 86% and dissociated in 14% of the 1,200 responses examined. The frequency of dissociation was dependent on the site in the esophagus and the frequency of vagal efferent stimulation (P less than 0.05). The interval between the onset of electrical and mechanical events, called electromechanical delay, had a regional gradient: 5 cm above LES greater than 3 cm greater than 1 cm (P less than 0.01). This delay was also dependent on the frequency of stimulation. The amplitude of spike burst and the number of spikes in a burst closely correlated with the amplitude of contraction. These studies show that electromechanical responses and dissociations are dependent on the regional level in the esophagus and the frequency of vagal stimulation.

The transmission mechanism of the vagal control of the feline pylorus.

Gastric motility and pyloric contractility were studied in laparotomized cats under chloralose anaesthesia by recording the intragastric volume and changes in an applied constant transpyloric flow of body-warm saline. Unilateralefferent electrical stimulation of the cervical vagi resulted in a prompt gastric contraction and a delayed pyloric contraction. In one third of the animals abiphasic pyloric motor response, consisting of a short period of increased flow preceding the longlasting decrease or cessation of the flow was observed. Afteratropine (0.2 mg/kg b.w.) the vagal nerve stimulation resulted in agastric relaxation, while the biphasic pyloric motor response was even more pronounced, with a significantly longer latency of the contractile phase. Addition ofguanethidine (2 mg/kg b.w.) did not affect these motor responses. Afterhexamethonium (25 mg/kg i.v. and 50±10 mg per kg i.a. b.w.) the stimulation procedure still resulted in a slight gastric relaxation, while the pyloric contraction was effectively blocked. However, the relaxatory phase required theaddition of atropine to become antagonized indicating separate transmission mechanisms for the relaxatory and contractile components of the pyloric motor response at efferent vagal stimulation.

A pharmacokinetic analysis of the vagal release of 5-hydroxytryptamine in the cat.

The kinetics of 5-hydroxytryptamine (5-HT) release into the portal system after efferent electrical vagal stimulation were studied in an in vivo model. Blood samples were drawn from cats before, during and after vagal nerve stimulation, and portal plasma levels of 5-HT were measured. Portal plasma concentration of 5-HT rose during stimulation. After termination of stimulation, the plasma levels returned to steady state values and were used to calculate half-life and elimination rate constant. When pharmacokinetic principles were applied, the plasma half-life (T1/2) was determined to be 1.32 min and the elimination rate constant (KE), 0.5246 min-1. Pharmacokinetic principles also were applied to data from earlier in vitro studies using exogenously administered 5-HT, and a half-life of 1.03 min and a KE of 0.67 min-1 were calculated. Therefore, it appears that exogenously administered 5-HT and neurogenically released endogenous 5-HT are metabolized at a similar rate, both having a short half-life.

The effect of propranolol on the serotonin concentration in the portal plasma after vagal nerve stimulation in the cat.

Efferent cervical vagal nerve stimulation in the cat caused a marked increase of the portal plasma 5-HT concentration. This increase was more than two-fold within 15 min of stimulation. After cessation of stimulation portal plasma 5-HT returned to basal levels within 10 min. Treatment with the beta-adrenoceptor antagonist propranolol, in various doses (0.1-2 mg/kg b.wt.), did not abolish but significantly reduced the response to vagal stimulation, particularly during the final part of the stimulation period. The results confirm the existence of a beta-adrenoceptor-mediated release of 5-HT, but also suggest that other mechanisms for 5-HT release may be involved in the response on vagal nerve stimulation.

The vagal control of the feline pyloric sphincter.

In acute experiments on cats in chloralose anesthesia the effects of efferent and afferent electrical stimulation of the cervical vagi on an applied constant flow of saline through the feline pylorus was studied. The motor activity of the stomach was recorded simultaneously with a volume recording technique. Efferent cervical vagal stimulation caused a decrease in the transpyloric flow and an increased gastric motor activity. In a few animals the decreased transsphincteric flow was preceded by a short period of increased flow. When the transpyloric flow was reduced by splanchnic nerve stimulation or a noradrenaline infusion, vagal nerve stimulation induced an increased flow through the pylorus indicating the presence of relaxatory fibres to the pylorus within the vagi. Electrical stimulation of the central end of the ipsilateral vagal nerve in the neck, with the contralateral vagal verve left intact, resulted in a decreased transpyloric flow and relaxation of the stomach. This response could be induced with or without intact splanchnic nerves, and disappeared when the intact contralateral vagus was cut. It is concluded that the vagi mediate both excitatory and inhibitory fibres to the pyloric sphincter in the cat. A vago-vagal excitatory reflex to the pylorus can be elicited by afferent vagal nerve stimulation together with a vago-vagal relaxatory response of the stomach.

The role of cardiac receptors in clonidine-induced vagal bradycardia

In chloralosed, spinalized and β-blocked cats, clonidine, 10 μg/kg i.v. caused a vagally mediated bradycardia which was further analysed with particular attention to cardiopulmonary receptors. Cardiovascular deafferention, with preservation of vagal cardial efferents, abolished the bradycardia. However, in animals with arterial baroreceptors denervated but with vagal cardiopulmonary pathways intact, clonidine decreased heart rate simultaneously with an increase in left atrial pressure to an extent known to activate cardiac receptors with unmyelinated vagal efferents. Clonidine somewhat enhanced the bradycardia to efferent vagal stimulation and also had a slight positive chronotropic effect on the non-innervated heart. The reflex bradycardia from electrical stimulation of unmyelinated cardiac afferents was augmented by the drug but not more than could be accounted for by the changed neuroeffector sensitivity. The data suggest that clonidine can reflexly augment vagal tone on the heart by an increased activity in vagal cardiac afferents, secondary to the drug's peripheral vasoconstrictor action, whereas no evidence for any central facilitation of these reflexes has been found.

VAGALLY INDUCED GASTRIC ANTRAL CONTRACTIONS AND GASTRIC EMPTYING OF A LIQUID TEST MEAL

The emptying of a liquid test meal from the stomach was studied during, and in the absence of, electrical stimulation of cut ends of a thoracic branch of the vagus in anaesthetized cats. The test meal (154 mmol.1-1 NaCl and 30 mg.1-1 phenol red) was measured by collecting effluent from a duodenal fistula over a 30 min period. The stomach emptied about 60% of the meal under control conditions compared with over 90% during efferent stimulation of the vagus. The increased volumes emptied during efferent stimulation were not accounted for by secretion of gastric acid. Coincident with the vagally evoked antral contractions there was a gush of liquid from the duodenal cannula. Afferent vagal stimulation resulted in an initial marked delay of emptying followed by an acceleration so that the volume emptied after 30 min was similar to that in control experiments. Antral contractions, evoked by efferent vagal stimulation, accelerated the emptying of a liquid test meal from the stomach.

Vagal control of lower oesophageal sphincter motility in the cat.

1. The effects of vagal efferent fibre stimulation on the smooth muscle of the lower oesophageal sphincter have been studied on the anaesthetized animal and on the isolated and perfused organ.2. In both muscle layers (longitudinal and circular) vagal stimulation elicits two types of electromyographic (e.m.g.) potentials: (a) excitatory junction potentials (e.j.p.s) where there is a depolarization of the smooth muscle fibres. E.j.p.s can give rise to spike potentials inducing a contraction of the sphincter; (b) inhibitory junction potentials (i.j.p.s) where there is hyperpolarization of the smooth muscle fibres, often followed by a transient depolarization which may initiate spikes (post-inhibitory rebound).3. Pure i.j.p.s are observed after atropine treatment which suppresses e.j.p.s. Under these conditions, a long lasting vagal stimulation induces a long duration hyperpolarization concomitant with an opening of the lower oesophageal sphincter followed after the cessation of stimulation by a powerful rebound leading to a strong contraction which closes the sphincter.4. Several arguments, pharmacological (action of acetylcholine (ACh), atropine and hexamethonium) and physiological (threshold and latency of responses) lead to the following conclusions. Preganglionic vagal fibres are cholinergic and they activate (a) intramural excitatory cholinergic neurones; (b) intramural non-adrenergic inhibitory neurones (purinergic neurones). Preganglionic fibres leading to inhibition have a higher threshold than those leading to excitation. Both excitatory and inhibitory pathways are interconnected inside the intramural network. In particular, activation of intramural inhibitory neurones, by relaxing the oesophagus orally to the lower oesophageal sphincter, inhibits intramural excitatory neurones and subsequently blocks vagal excitatory responses.5. Two functions may be attributed to the vagal extrinsic innervation: (a) closure of the lower oesophageal sphincter by maintaining the basal tone of the sphincter; this would imply that at rest the inhibitory control is supplanted by the excitatory one; (b) sphincter opening during swallowing by suppressing the excitatory stimulus and reinforcing the inhibitory one (it may be recalled that after bilateral vagotomy, swallowing is no longer followed by a relaxation of the sphincter).

A possible vagal adrenergic release of serotonin from enterochromaffin cells in the cat.

The intracellular concentrations of serotonin (5-HT) in enterochromaffin cells (EC) in the cat small intestine have been studied by a cytofluorimetric method before and after long-lasting efferent vagal nerve stimulation in the neck. Such stimulation induces a decrease of 5-HT in EC of the gut as observed previously. Pretreatment with atropine could not block this decrease, suggesting a noncholinergic mechanism. Pretreatment with a beta-blocking agent, propranolol, or bilateral removal of the superior cervical ganglia could, however, block this 5-HT decrease. Pretreatment with an alpha-blocking agent, phenoxybenzamine, caused an increase in the 5-HT content of EC both with and without nerve stimulation; the reason for this is obscure. The results indicate, that vagal nerve stimulation induces a neurogenic 5-HT release from EC in the gut, and that adrenergic fibres, originating in the superior cervical ganglia, mediate this release probably via a beta-receptor mechanism. Whether or not an alpha-receptor mechanism is also involved cannot be judged at present.

Cardiac receptors in ducks--a link between vasoconstruction and bradycardia during diving.

It has been demonstrated that cardiac receptors, most likely of the left ventricular type, are present also in the duck's heart. These receptors and their reflex responses (i.e. bradycardia and hypotension) could be blocked by intrapericardial administration of lidocaine. Initially, usch receptor blockade did not affect efferent vagal control of heart rate, as revealed by undiminished bradycardia in response to a standardized vagal stimulation. After cardiac receptor blockade, however, the duck's normal bradycardia response to head immersion was greatly reduced. The cardiovascular response to submersion was now instead characterized by a marked rise in arterial pressure, with superimposed bouts of intensified bradycardia and pressure reduction, evidently induced reflexly from the arterial baroreceptors. Meanwhile, the bradycardia response to standarized efferent vagal stimulation was still the same as before intrapericardial lidocaine injection. These results suggest that the marked rise in cardiac filling pressure following the intense shemo-receptor-induced constriction of both resistance and capacitance vessels, activates ventricular stretch receptors signalling in vagal afferents. Apparently, the activation of these receptors contributes crucially to the bradycardia and reduction of cardial output, which balance off the greatly increased peripheral resistance in the diving duck.

The vagal control of the ileo-cecal sphincter in the cat.

In acute experiments on chloralosed cats the effect of efferent cervical vagal stimulation on a flow through the ileo-cecal sphincter (ICS) was studied. The motor activity of the jejunum, ileum and large intestine adjacent to the sphincter was recorded simultaneously. Vagal stimulation caused a decrease in the transphincteric flow and increased motor activity in the ileum. Increased motor activity in the proximal colon was recorded only occasionally. When the vagal nerves were stimulated during continuous splachine stimulation the transsphincteric flow was decreased although the tone and motility of the ileum was suppressed. Furthermore, guanethidine (1-3 mg/kg b.w.) blocked or suppressed the effect of vagal stimulation on the transsphincteric flow while the excitatory response of the proximal colon was greatly enhanced. This indicates that the reduction of the transsphinctteric flow following vagal stimulation was at least partly due to a direct effect of the vagal nerves on the sphincteric muscle and not to a squeezing effect of that part of the colonic wall that surrounds the sphincter. Atropine (0.1 and 1 mg/kg b.w.) blocked all responses to vagal stimulation. Thus, both guanethidine and atropine blocked the vagally induced contraction of the ICS. Relaxation to the ICS was never obtained by vagal stimulation even when the tone of the sphincter had been increased by infusion of noradrenaline.

Changes in regional vascular resistance after myocardial infarction in the dog

The possibility that failure of vascular resistance to increase during hypotension in cardiogenic shock is a generalized phenomenon affecting many vascular beds was investigated in anesthetized dogs subjected to coronary arterial embolization. Blood flow in the carotid, mesenteric and renal vascular beds was monitored. Efferent vagus nerve stimulation, which, through bradycardia, produces hypotension of cardiac origin without myocardial damage, was associated with reflex vasoconstrictor responses in the carotid and mesenteric vascular beds; no change in resistance occurred in the renal vascular bed. In marked contrast, vasoconstriction failed to occur in any of the vascular beds in response to the hypotension produced by coronary embolization. These responses to cardiogenic shock mimicked those seen after ganglionic blockade, in which hypotension of partly cardiac origin was produced and reflex vasoconstriction blocked. The data support the previous hypothesis that myocardial infarction is associated with reflex inhibition of the reflex vasoconstrictor response to hypotension.

Vagal relaxation of the stomach induced by apomorphine in the cat.

AbstractIn anesthetized or decerebrate unanesthetized cats administration of the emetic drug apomorphine produced pronounced and long‐lasting relaxation of the stomach. When apomorphine induced somatomotor retching or vomiting movements they were always preceded by gastric relaxation. The gastric relaxatory response to apomorphine could not be blocked by atropine or guanethidine but was completely abolished after vagotomy. Vagotomy, if performed during the relaxed state of the stomach after apomorphine administration, resulted in a prompt decrease of gastric volume. Injection of apomorphine had no essential effect on gastric contractions induced by efferent electrical vagal stimulation, indicating that the splanchnic nerves were of minor or no importance for the apomorphine induced gastric relaxation.—It is concluded that the emetic drug apomorphine produces gastric relaxation by activation of the vagal non‐adrenergic relaxatory nerve fibres to the stomach. The results indicate that the relaxation of the proximal part of the stomach known to appear early in the vomiting act, is mediated by these relaxatory nerve fibres.

Effects of altering ventricular rate on blood flow distribution in conscious dogs.

Effects of altering ventricular rate on blood flow distribution in conscious dogs.

The effect of vagotomy, vagal cooling and efferent vagal stimulation on breathing and lung mechanics of rabbits.

1. The effects of bilateral cervical vagotomy, of bilateral vagal cooling and of efferent vagal stimulation were studied on rabbits anaesthetized with pentobarbitone sodium. Total lung conductance, lung compliance, breathing frequency, tidal volume, end-tidal CO(2)%, systemic arterial and right atrial blood pressures and heart rate were measured. Some of the rabbits were first paralysed and artificially ventilated.2. The changes in lung conductance were consistent with the presence of a tonic efferent vagal discharge in bronchoconstrictor fibres, reflexly damped down by a tonic afferent vagal discharge dilator to the airways, probably the Hering-Breuer inflation reflex.3. Neither vagotomy nor efferent vagal stimulation significantly influenced lung compliance, right atrial pressure or end-tidal CO(2)%; vagal cooling lowered end-tidal CO(2)% in spontaneously breathing rabbits, but did not affect the other variables.4. Efferent vagal stimulation in the rabbit decreased lung conductance with no significant change in lung compliance.5. In the rabbit, vagal efferent activity affects primarily the larger (resistance) air passages with little action on the distal (compliance-influencing) airways.

Influence of efferent vagal stimulation of left ventricular function in dogs.

Influence of efferent vagal stimulation of left ventricular function in dogs.

Effects of efferent vagal stimulation on atrial and ventricular function.

ARTICLESEffects of efferent vagal stimulation on atrial and ventricular functionMA Harman, and TJ ReevesMA Harman, and TJ ReevesPublished Online:01 Nov 1968https://doi.org/10.1152/ajplegacy.1968.215.5.1210MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNeurophysiology of Heart16 June 2020Vagus Nerve Stimulation for the Treatment of Heart FailureIntermittent electrical stimulation of the right cervical vagus nerve in salt-sensitive hypertensive rats: effects on blood pressure, arrhythmias, and ventricular electrophysiology11 August 2015 | Physiological Reports, Vol. 3, No. 8Vagal Stimulation for Heart FailureMyths and realities of the cardiac vagus14 August 2013 | The Journal of Physiology, Vol. 591, No. 17Baroreflex Activation for the Treatment of Heart Failure20 April 2012 | Current Cardiology Reports, Vol. 14, No. 3Vagus nerve stimulation in experimental heart failure3 December 2010 | Heart Failure Reviews, Vol. 16, No. 2The effect of direct autonomic nerve stimulation on left ventricular force in the isolated innervated Langendorff perfused rabbit heartAutonomic Neuroscience, Vol. 124, No. 1-2Hemodynamic significance of heart rate in neurally mediated syncope5 December 2006 | Clinical Cardiology, Vol. 27, No. 11Decreased Contractility of the Left Ventricle is Induced by the Neurotrausmitter Acetylcholine, but not by Vagal Stimulation in Rats.Japanese Heart Journal, Vol. 44, No. 2The Dose-Dependent Effects of Halothane on Right Ventricular Contraction Pattern and Regional Inotropy in SwineAnesthesia & Analgesia, Vol. 82, No. 6Autonomic influences on regional cardiac [14C] 2-deoxyglucose uptake in paced dog heartBasic Research in Cardiology, Vol. 86, No. 6A simple experimental index for the evaluation of inotropic responsesJournal of Pharmacological Methods, Vol. 18, No. 1The hemodynamic effects of sympathetic stimulation combined with parasympathetic blockade in man.Circulation, Vol. 75, No. 5A Biofeedback Controller Unit2 June 2015 | IETE Technical Review, Vol. 3, No. 10Autonomic Reflex Control of Cardiac ContractilityThe distribution of acetylcholine and choline in guinea pig heartLife Sciences, Vol. 36, No. 4Autonomic mechanisms regulating myocardial contractility in conscious animalsPharmacology & Therapeutics, Vol. 29, No. 2Pressor and depressor responses after cholinergic blockade in humansAmerican Heart Journal, Vol. 107, No. 5Carotid dP/dt as a Psychophysiological Index of Sympathetic Myocardial Effects: Some ConsiderationsPsychophysiology, Vol. 17, No. 5Cardiac responses during stimulation of the dorsal motor nucleus and nucleus ambiguus in the cat.Circulation Research, Vol. 46, No. 5Asystole and its treatment: The possible role of the parasympathetic nervous system in cardiac arrestJournal of the American College of Emergency Physicians, Vol. 8, No. 11Vagal control of coronary blood flow in dogsBasic Research in Cardiology, Vol. 74, No. 3Baroreflex and vagal mechanisms modulating left ventricular contractile responses to sympathomimetic amines in conscious dogs.Circulation Research, Vol. 44, No. 2Effect of vagal stimulation on the overflow of norepinephrine into the coronary sinus during cardiac sympathetic nerve stimulation in the dog.Circulation Research, Vol. 38, No. 2Stable T wave effects during improvement of heart rate control with biofeedbackPhysiology & Behavior, Vol. 16, No. 1Reflex parasympathetic coronary vasodilation elicited from cardiac receptors in the dog.Circulation Research, Vol. 37, No. 2A Cardiocardiac Sympathovagal Reflex in the CatCirculation Research, Vol. 32, No. 2Functional, metabolic and structural studies of the chronic canine cardiac autotransplantJournal of Surgical Research, Vol. 13, No. 6Reflex changes in cardiac vagal efferent nervous activity elicited by stimulation of afferent fibres in the cardiac sympathetic nervesBrain Research, Vol. 42, No. 2Adrenergic and cholinergic blockade of cardiovascular responses to subcortical electrical stimulation in unanesthetized rabbitsPhysiology & Behavior, Vol. 8, No. 5Cardiac Innervation and Synaptic Transmission in HeartHerzParasympathetic Control of Coronary Blood Flow in DogsCirculation Research, Vol. 25, No. 5Positive and Negative Inotropic Responses of the Atria and Ventricles to Vagosympathetic Stimulation in the Isovolumic Canine HeartCirculation Research, Vol. 25, No. 3Inotrope Wirkungen des Nervus Vagus am Hundeventrikel in situPfl�gers Archiv European Journal of Physiology, Vol. 310, No. 1 More from this issue > Volume 215Issue 5November 1968Pages 1210-1217 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.215.5.1210PubMed5687515History Published online 1 November 1968 Published in print 1 November 1968 Metrics