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PubMed1996

Different vagal modulation of the sinoatrial node and AV node in patients with congestive heart failure.

1. We have previously shown that in healthy young men autonomic control of the sinoatrial (SA) and AV node may be independent during sleep. It is conceivable, that this independence is lost in patients with high sympathetic activity. This would be in analogy to exercise in normal subjects, where an increase in sinus rate is associated with a shortening of the PR interval. 2. The aim of this study was to investigate whether this independence of SA and AV nodal autonomic modulation is maintained in patients with congestive heart failure. 3. For analysis of heart rate variability (HRV) the ECG was online digitized from 10 pm to 6 am in six patients with congestive heart failure (EF < 40%). The onset of P-waves and QRS-complexes was recognized by a computer algorithm with an accuracy of +/-1 ms. Power spectra of PR intervals and PP intervals were calculated for consecutive 256 second segments. The power in the high frequency component. (HF, 0.15 - 0.4 Hz) of PP intervals was used as an index of vagal drive to the SA node. The vagal input to the AV node was determined by the spectral power of the corresponding PR intervals. 4. All patients showed the typical spectral peak in the HF band, both in PP and PR. The power spectral density of HF varied over time with different patterns for PP and PR. The ratio of the HF power derived from PP and PR was calculated for each segment. This ratio was not constant, but showed a distinct time course. 5. Congestive heart failure did not abolish the independence of vagal modulation of SA and AV node, as assessed by the HF power derived from PP and PR intervals. Thus, the difference in vagal traffic to the SA and AV node was maintained even in the setting of high background sympathetic activity. Further investigation is needed to analyze potential factors responsible for this difference in patterns and the clinical relevance of this finding.

Adult↗
PubMed2006

Vagal modulation and aging.

Cardiovascular disease accounts for approximately 30% of all deaths worldwide, and will only worsen as the world's population ages. It is well-established that age, per se, is a major risk factor and contributor to all cardiovascular morbidities and mortalities. However, environmental factors, including a lack of exercise, appear to play a critical role in the onset and progression of cardiovascular disease. This paper reviews the literature on cardiac variability and aging and addresses risk factors associated with aging that can be modified and possibly attenuate the decline of heart rate variability with aging, including exercise training to increase vagal modulation. Thus, results of the studies described in this review support a potential benefit of increasing or maintaining fitness in order to slow the decline of parasympathetic control of HR with normal aging.

Adaptation, Physiological↗
PubMed2006

Early occurrence of anti-muscarinic autoantibodies and abnormal vagal modulation in Chagas disease.

BACKGROUND: Autoimmunity and dysautonomia are established features of Chagas disease (ChD) that could be related to its pathogenesis. Our objective was to assess heart rate variability (HRV) and levels of anti-M2 receptors autoantibodies in ChD patients with and without left ventricular (LV) dysfunction, in order to establish if these abnormalities occur early and concomitantly in the course of the illness. METHODS: ChD patients (n=75) and healthy controls (n=14) underwent a standardized protocol including Doppler echocardiogram, Holter monitoring, HRV analysis, and measurement of anti-M2 receptors autoantibodies (ELISA). ChD patients were divided accordingly by the absence (group 1, n=45) or presence (group 2, n=30) of LV dysfunction, defined as reduced LV ejection fraction (<55%) or regional wall motion abnormalities (including ventricular aneurysm). RESULTS: Both ChD groups displayed increased optical density values of anti-M2 cholinergic autoantibodies (Median (IQR): control=1.98(0.51); ChD 1=2.76(0.97); ChD 2=2.72(1.34), p<.001) and reduced HF power of spectral analysis of HRV when compared to controls (Median (IQR) in ms2: control=1087(2284); ChD 1=286(763); ChD 2=285(763), p<.001). M2 levels were significantly correlated with HF power values (r=-0.32, p=0.023), but not with LV ejection fraction. CONCLUSIONS: Anti-muscarinic autoantibodies and abnormal vagal modulation occur early in ChD patients, independently of the presence of LV dysfunction. Levels of antibodies against M2 muscarinic receptors were significantly and negatively correlated with HRV index HF power, suggesting an inhibitory effect of autoantibodies in vagal function.

Adult↗
PubMed2004

Restoration of heart rate turbulence by titrated beta-blocker therapy in patients with advanced congestive heart failure: positive correlation with enhanced vagal modulation of heart rate.

INTRODUCTION: Heart rate turbulence (HRT) is a powerful novel predictor for cardiovascular mortality. Chronic congestive heart failure is associated with abnormal HRT. Whether antiadrenergic beta-blocker therapy can restore control of HRT in patients with chronic congestive heart failure is unknown. METHODS AND RESULTS: A 24-hour Holter ECG recording was obtained before and 1 and 3 months after titrated addition of atenolol therapy in 10 consecutive patients with advanced congestive heart failure. Two parameters derived from HRT, turbulence slope (TS) and turbulence onset (TO), and time- and frequency-domain heart rate variability (HRV) parameters (SDNN, RMSSD, VLF, LF, HF) from 24-hour ECG were compared before and after beta-blocker therapy, together with the same parameters in age-matched normal control. Results showed that TS (3.1 +/- 2.2 vs 6.2 +/- 3.0; P = 0.001) and all HRV parameters were increased after 3 months of atenolol treatment. No changes in TO were evident (0.6 +/- 0.5 vs -0.2 +/- 1.3; P = 0.13). The improvement of TS and the vagally mediated parameters of mean R-R interval, RMSSD, and the HF component of HRV were positively correlated. CONCLUSION: Abnormal HRT caused by chronic congestive heart failure can be restored by beta-blocker therapy. The evolution of TS was positively correlated with measures of vagal modulation of heart rate.

Adrenergic beta-Antagonists↗
PubMed2006

Hyperthyroidism is characterized by both increased sympathetic and decreased vagal modulation of heart rate: evidence from spectral analysis of heart rate variability.

OBJECTIVE: The clinical manifestations of hyperthyroidism resemble those of the hyperadrenergic state. This study was designed to evaluate the impact of hyperthyroidism on the autonomic nervous system (ANS) and to investigate the relationship between serum thyroid hormone concentrations and parameters of spectral heart rate variability (HRV) analysis in hyperthyroidism. DESIGN AND PATIENTS: Thirty-two hyperthyroid Graves' disease patients (mean age 31 years) and 32 sex-, age-, and body mass index (BMI)-matched normal control subjects were recruited to receive one-channel electrocardiogram (ECG) recording. MEASUREMENTS: The cardiac autonomic nervous function was evaluated by the spectral analysis of HRV, which indicates the autonomic modulation of the sinus node. The correlation coefficients between serum thyroid hormone concentrations and parameters of the spectral HRV analysis were also computed. RESULTS: The hyperthyroid patients revealed significant differences (P < 0.001) compared with the controls in the following HRV parameters: a decrease in total power (TP), very low frequency power (VLF), low frequency power (LF), high frequency power (HF), and HF in normalized units (HF%); and an increase in LF in normalized units (LF%) and in the ratio of LF to HF (LF/HF). After correction of hyperthyroidism in 28 patients, all of the above parameters were restored to levels comparable to those of the controls. In addition, serum thyroid hormone concentrations showed significant correlations with spectral HRV parameters. CONCLUSIONS: Hyperthyroidism is in a sympathovagal imbalanced state, characterized by both increased sympathetic and decreased vagal modulation of the heart rate. These autonomic dysfunctions can be detected simultaneously by spectral analysis of HRV, and the spectral HRV parameters could reflect the disease severity in hyperthyroid patients.

Adult↗
PubMed2005

Impaired vagal modulation of heart rate in individuals with Down syndrome.

The attenuated heart rate (HR) and blood pressure (BP) response to exercise in individuals with Down syndrome (DS) has been attributed to autonomic dysfunction, which has been associated with obesity. Our purpose was to determine the role of autonomic control of HR to the attenuated chronotropic response observed in individuals with DS. We evaluated spectral analysis of HR variability (HRV) in 13 individuals with (BMI 32+/-5 kg/m(2), P<0.05) and 14 without DS (BMI 26+/-3 kg/m(2)) by means of 2 min isometric handgrip at 30% of maximal force followed by recovery. Noninvasive measures of HR (ECG) and systolic BP (SBP) (Portapres) were recorded continuously. The increases in HR and SBP, and decrease in high frequency (HF) component were significantly greater in controls than in individuals with DS (P<0.05) during handgrip. The increase in LF/HF ratio was not significantly affected by handgrip and was comparable in both groups. During recovery, the decreases in HR, SBP, and LF/HF ratio, and the increase in HF were significantly greater in controls than in individuals with DS (P<0.05). Controlling for BMI did not alter these results. The attenuated HR and SBP response to the handgrip test in individuals with DS is explained by blunted vagal modulation. Our study suggests that autonomic dysfunction in individuals with DS might be independent of obesity.

Adolescent↗
PubMed2003

Vagal modulation of bradykinin-induced mechanical hyperalgesia in the female rat.

In male rats, activity in subdiaphragmatic vagal afferents modulates nociception via an adrenal medulla-dependent mechanism. Because both the vagus and adrenal medullae are sexually dimorphic, we evaluated vagotomy-induced changes in mechanical nociceptive threshold and inflammatory hyperalgesia in female rats and compared them to those previously reported in male rats. We have found that (1) mechanical nociceptive threshold is lower in female rats than in male rats, perhaps because of tonic release of adrenal medullary factors in female rats; (2) mechanical nociceptive threshold in female rats is influenced to a lesser degree by activity in the subdiaphragmatic vagus; (3) vagotomy-induced enhancement of bradykinin hyperalgesia is greater in female rats; (4) in female rats, in contrast to male rats, celiac plus celiac accessory branch vagotomy failed to fully account for the enhancement of bradykinin hyperalgesia in complete subdiaphragmatic vagotomy; and (5) in female rats, in contrast to male rats, adrenal medullectomy plus subdiaphragmatic vagotomy only partially (approximately 30%) reversed the effect of vagotomy on bradykinin hyperalgesia. These findings demonstrate sexual dimorphism in the modulation of both mechanical nociceptive threshold and bradykinin-induced hyperalgesia by activity in subdiaphragmatic vagal afferents as well as the adrenal medulla.

Adrenal Medulla↗
PubMed2004

Low-dose atropine amplifies cardiac vagal modulation and increases dynamic baroreflex function in humans.

It has been previously known that low-dose atropine (LDA) enhances vagal outflow to the heart. To demonstrate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability, we evaluated the effect of vagal cardiac stimulation with administration of LDA on ABP fluctuation during dynamic hypertensive and hypotensive stimuli. We assessed changes in RR interval (RRI), ABP, power spectral densities of heart rate variability (HRV) and ABP variability, and spontaneous baroreflex sensitivity (BRS) in 16 healthy volunteers before and after administration of LDA (2 microg/kg). Transient hypertension was induced by phenylephrine (2 microg/kg), whereas hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. LDA elicited bradycardia and significantly increased high-frequency (HF, 0.15-0.4 Hz) power of HRV and spontaneous BRS, as determined by transfer function analysis. The increase in systolic blood pressure (SBP) after phenylephrine administration was significantly attenuated by LDA (16+/-2 to 11+/-3 mmHg, P<0.005) and was associated with the augmented reflex bradycardia, whereas the decrease in SBP after cuff deflation was not affected (14+/-5 to 13+/-5 mmHg) with the augmented reflex tachycardia. Increases of HF HRV were correlated significantly and negatively with the increased SBP induced by phenylephrine before and after LDA (r=-0.502, P<0.05). These data suggest that the increased vagal cardiac function induced by LDA augments HR buffering effects, and is important in minimizing arterial pressure fluctuation during dynamic hypertensive stimuli.

Adult↗
PubMed2003

Vagal modulation of nociception is mediated by adrenomedullary epinephrine in the rat.

Vagal afferent activity modulates mechanical nociceptive threshold and inflammatory mediator-induced hyperalgesia, effects that are mediated by the adrenal medulla. To evaluate the role of epinephrine, the major hormone released from the adrenal medulla, the beta2-adrenergic receptor antagonist ICI 118,551 was chronically administered to vagotomized rats and epinephrine to normal rats. In vagotomized rats, chronic administration of ICI 118,551 markedly attenuated vagotomy-induced enhancement of bradykinin hyperalgesia but had no effect on nociceptive threshold. In normal rats, chronic epinephrine had the opposite effect, enhancing bradykinin hyperalgesia. Like vagotomy-, epinephrine-induced enhancement of hyperalgesia developed slowly, taking 14 days to reach its peak. Vagotomy induced a chronic elevation in plasma concentrations of epinephrine. We suggest that ongoing activity in vagal afferents inhibits the release of epinephrine from the adrenal medulla. Chronically elevated levels of epinephrine, occurring after vagotomy, desensitize peripheral beta2-adrenergic receptors and lead to enhancement of bradykinin hyperalgesia. The ability of prolonged elevated plasma levels of epinephrine to sensitize bradykinin receptors could contribute to chronic generalized pain syndromes.

Adrenal Medulla↗
PubMedDate not supplied

Muscarinic cholinergic receptors modulate vagal cardiac responses in man.

Respiratory sinus arrhythmia (peak-valley P-P interval changes during controlled breathing) and carotid baroreceptor-cardiac reflex responses (provoked by neck suction) were studied before and after low (0.725 microgram/kg) or high (0.043 mg/kg) dose atropine sulfate infusions in 22 healthy young adults. There was a highly significant (r = 0.78, P = 0.002) correlation between resting respiratory sinus arrhythmia and baroreflex responses. Low dose atropine increased the magnitude of sinus arrhythmia and baroreflex responses. Large dose atropine reduced sinus arrhythmia and baroreflex responses in an exponential fashion. Our results link respiratory sinus arrhythmia with baroreflex responsiveness and provide inferential evidence that vagal cardiac efferent activity is modulated by inhibitory cholinergic receptors. We speculate that blockade of these receptors by low doses of atropine amplifies vagal motoneuron responses to incoming baroreceptor information, and thereby increases average maximum and minimum levels of vagal cardiac outflow during breathing.

Adult↗
PubMed2000

Pulmonary vagal modulation of ventilation in toads (Bufo marinus).

This study examined the role of pulmonary vagal feedback on hypercapnic chemosensitivity and breathing pattern formation in cane toads (Bufo marinus). Decerebrate, paralysed toads were uni-directionally ventilated with air, 2.5% CO(2) or 5.0% CO(2) with the lungs inflated or deflated, before and after pulmonary vagotomy. Motor output from the mandibular branch of the trigeminal nerve served as an index of fictive breathing. As respiratory drive was increased, breathing frequency increased and breaths were clustered into discrete episodes separated by periods of apnea. Lung deflation tended to enhance episodic breathing while inflation biased the system towards apnea at low levels of respiratory drive and a pattern of continuous, small breaths at higher levels of respiratory drive. Following bilateral pulmonary vagotomy there was no increase in ventilation during hypercapnia and lung inflation/deflation had no effect on breathing pattern. In isolated brainstem-spinal cord preparations from the same animals, all variables associated with fictive breathing were unaffected by changes in superfusate pH from 8.0 to 7.6. The breathing pattern from the in vitro preparations was highly variable. This study demonstrates a crucial role for vagal feedback in modulating respiration and the respiratory responses to hypercapnia in B. marinus.

Animals↗
PubMed2003

Vagal modulation of spinal nicotine-induced inhibition of the inflammatory response mediated by descending antinociceptive controls.

Noxious stimuli activate neuroendocrine axes, inhibiting inflammation, an effect that is powerfully attenuated by ongoing activity in subdiaphragmatic vagal afferents. To evaluate whether this inhibitory effect of vagal afferent activity is mediated by descending antinociceptive control, we tested whether antagonizing descending antinociceptive controls: (i) enhances the inhibition of inflammation produced by spinal nicotine (which stimulates central terminals of nociceptors) and (ii) occludes the enhancing effect of subdiaphragmatic vagotomy, in the rat. Spinal intrathecal co-administration of the alpha-adrenergic receptor antagonist phentolamine and the non-selective opioid receptor antagonist naloxone, and acute subdiaphragmatic vagotomy each produced enhancement, with similar magnitude, of nicotine-induced inhibition of plasma extravasation, produced by the potent inflammatory mediator, bradykinin. The combination of subdiaphragmatic vagotomy and intrathecal receptor antagonists, however, produced no further enhancement compared to each treatment alone. These findings support the suggestion that activity in descending antinociceptive controls modulates noxious stimulus-induced inhibition of inflammation and the vagal modulation of noxious stimulus-induced inhibition of inflammation is mediated by descending antinociceptive controls.

Adrenergic alpha-Antagonists↗
PubMed1998

Vagal modulation of ventricular tachyarrhythmias induced by left ansae subclaviae stimulation in rabbits.

Previous evidence has shown that vagal nerve activity modulates ventricular arrhythmias in patients and in animal models. However, the effects of direct vagus nerve stimulation on ventricular tachyarrhythmias brought by direct sympathetic nerve stimulation have not been elucidated. In the present study, the effects of electrical stimulation of the left cervical vagus nerve on ventricular tachycardia (VT) which was induced by electrical stimulation of the left ansae subclaviae (LAS) in rabbits were assessed. Monophasic action potentials (MAPs) of the left ventricular endocardium were recorded simultaneously with surface ECG. In 27 rabbits tested, the stimulation of LAS induced VT in 19 rabbits. Polymorphic VT (PVT) was induced in 14 rabbits (PVT group), whereas monomorphic VT (MVT) was induced in 5 rabbits (MVT group). Vagus nerve stimulation during the sympathetically-induced PVT led to a restoration of sinus rhythm in 10 of 14 rabbits, while that during the sympathetically-induced MVT did not restore sinus rhythm in any of the 5 rabbits. Vagus nerve stimulation during the stimulation of LAS, which was of subthreshold intensity for the induction in VT, did not result in an induction of PVT in any of the 14 rabbits in the PVT group, while it induced slow MVT in 3 of 5 rabbits in the MVT group. These results indicate that vagus nerve stimulation preferentially exerts protective antiarrhythmic effects against PVT induced by sympathetic neural stimulation in this model, while it occasionally induces slow MVT under conditions in which sympathetic nerve activity in potentially elevated.

Animals↗
PubMed2001

Gender and gonadal hormone effects on vagal modulation of tonic nociception.

We studied the influence of gender and gonadal hormones on modulation of tonic nociception exerted by vagal activity. In male rats, subdiaphragmatic vagotomy resulted in significantly reduced nociceptive behavior during phase 2 of the formalin test. Whereas gonadectomy alone had no effect, it completely eliminated the suppressive effect of subdiaphragmatic vagotomy; however, sex hormone replacement with either testosterone or dihydrotestosterone did not restore the ability of subdiaphragmatic vagotomy to suppress nociceptive behavior. These results suggest that, in males, a gonad-dependent but androgenic gonadal hormone-independent mechanism contributes to pronociceptive effects of vagal afferent activity. Although neither gonadectomy nor subdiaphragmatic vagotomy alone affected the response to formalin in females, gonadectomy plus vagotomy resulted in significantly reduced nociceptive behavior during phase 2. Reconstitution with 17 beta-estradiol implants in gonadectomized females not only prevented suppression of nociceptive behavior seen with gonadectomy plus vagotomy, but also led to increased nociceptive behavior in the interphase between phases 1 and 2. However, placement of 17 beta-estradiol implants in gonad-intact females had no effect on formalin-induced nociceptive behavior. The finding that estrogen produced an increase in nociceptive behavior in gonadectomized female rats after vagotomy but not in normal female rats (with intact gonads and subdiaphragmatic vagus) suggests that the interaction between estrogen and nociceptive afferent activity is suppressed by vagal function. In conclusion, a nonandrogenic action of testicular function in male rats and estrogen in females seems to influence the effect of vagal activity on formalin-induced nociceptive behavior.

Journal Article↗
PubMed1999

Vagal modulation of responses elicited by stimulation of the aortic depressor nerve in neurons of the rostral ventrolateral medulla oblongata in the rat.

Stimulation of cervical vagal afferents inhibits central sympathetic outflows in part by inhibiting the ongoing activity of putative baroreceptive neurons in the rostral ventrolateral medulla oblongata. The aim of the present study was to examine the electrophysiological characteristics of vagal responses and their interactions with responses elicited by stimulation of the aortic nerve in neurons there. The study focused on the role of the long-lasting, late-onset vagal inhibition, which is likely to play an important role in the tonic inhibitory effects of vagal afferent stimulation. In vivo intracellular recordings were obtained from 33 neurons that received convergent inputs from aortic and vagal afferents. Sixty-four percent of these neurons exhibited a late inhibition following electrical stimulation of myelinated vagal afferents (mean onset latency of 100+/-5 ms). The average duration of late inhibition (294+/-19 ms) exceeded the duration of the cardiac cycle. As a consequence of this, sustained vagal stimulation diminished the effect of rhythmic baroreceptor inputs in neurons that exhibited late vagal inhibition. Simultaneous activation of aortic and vagal afferents significantly increased the magnitude of late inhibition, even in those neurons where stimulation of the aortic nerve alone did not elicit a response (n = 15). This suggested that the convergence between vagal and aortic afferent inputs occurred in inhibitory inteneurons antecedent to the recorded rostral ventrolateral medulla oblongata neurons. Focal stimulation of the caudal part of the nucleus of the solitary tract also elicited a late-onset inhibition in 73% of the neurons that responded to stimulation of the aortic nerve. This inhibition appeared to be similar to the late vagal inhibition, except for its shorter average onset latency (64+/-7 ms). Based on this observation, it is proposed that inhibitory inteneurons that mediate late inhibition to rostral ventrolateral medulla oblongata neurons may lie within the caudal part of the nucleus of the solitary tract. The present study established that activation of myelinated vagal afferents exerts a complex modulation over the ongoing and evoked activity of neurons that respond to stimulation of the aortic nerve. The complex interaction that occurs between aortic and vagal inputs in neurons of the rostral ventrolateral medulla may be implicated in long-term modulation of sympathetic outflows in response to changes in the activation of visceral receptors supplied by vagus afferents. The modulation elicited by late vagal inhibition may help to adjust cardiovascular outflows according to requirements set by the thoraco-abdominal visceral environment.

Animals↗
PubMed2001

Afferent vagal modulation. Clinical studies of visceral sensory input.

UNLABELLED: The frequency composition of a continuous time series of R-R intervals may be viewed as the phasic output of a central processing system intimately dependent on sensory input from a variety of afferent sources. While different measures of heart rate variability permit a glimpse into the autonomic efferent limb of this complex system, direct access of afferent fibers in humans has remained elusive. Using a specially designed esophageal catheter/manometer probe, we have been able to gain access to vagal afferent fibers in the distal esophagus. Our studies on the effect of vagal afferent electrostimulation on both cerebral evoked potentials (EvP) and the power spectrum of heart rate variability have yielded the following observations: 1. Stimulation of esophageal vagal afferents dramatically and reproducibly increases the high frequency (HF) vagal power and reduces the low frequency (LF) power of the heart rate autospectrum. 2. This effect is constant across stimulation frequencies from 0.1 to 1.0 Hz and across stimulation intensities from 2.5 to 20 mA. 3. Regardless of the stimulation parameters, there are only minimal changes in heart rate (2-6 bpm) and no change in respiratory frequency. 4. There is a linear correlation between electrical stimulation intensity and the amplitude of cerebral evoked potentials, whereas there is a non-linear relationship with all short-term power spectral indices. 5. While cerebral evoked potentials are only elicited at stimulation intensities above perception threshold, there is already a significant shift to increased vagal efferent modulation well below perception threshold. CONCLUSION: These studies support the concept that power spectral indices of heart rate variability represent phasic output responses to tonic afferent viscerosensory signals in humans. These studies also demonstrate the feasibility of accessing vagal afferents in humans.

Evoked Potentials, Somatosensory↗
PubMed1993

Hepatic glucose signals vagally modulate the cyclicity of gastric motility in rats.

The cyclicity and intensity of gastric motility were examined following glucose injection into the portal vein with an intragastric balloon in anesthetized rats. Enhanced gastric motility caused by insulin administration was influenced by 4 mM glucose (25 microliters) injected into the portal vein; glucose provoked a shift in the cyclicity power spectrum without any change in intensity. The peak power spectrum shifted from 4.0-5.0 cpm to 2.0-3.0 cpm. Hepatic branch vagotomy abolished the response. The results suggest that glucose signals in the hepatic vagal branch modulate the cyclicity of gastric motility.

Animals↗
PubMed1990

Vagal modulation of the rate-dependent properties of the atrioventricular node.

Vagal effects on atrioventricular (AV) nodal conduction are accentuated by increases in heart rate. To establish the mechanism of these rate-dependent negative dromotropic actions, we studied the properties governing AV nodal adaptation to changes in heart rate in chloralose-anesthetized dogs in the absence and presence of bilateral cervical vagal nerve stimulation (20 Hz, 0.2 msec). Stimulation protocols were applied to evaluate the contributions of changes in AV nodal recovery, facilitation, and fatigue independently of each other. Vagal stimulation slowed AV nodal recovery in a voltage-dependent way, increasing the time constant of recovery (tau r) from 80 +/- 7 to 194 +/- 16 msec (mean +/- SEM, p less than 0.01) at the highest voltage studied. The facilitating effect of a premature (A2) beat was manifested by a leftward shift of the recovery curve (A3H3 versus H2A3) of a subsequent A3 beat. The magnitude of shift depended on the A1A2 coupling interval and was reduced by vagal stimulation at all A1A2 intervals (maximum shift: control, 63 +/- 12 msec; vagus, 24 +/- 11 msec; p less than 0.01). When recovery and facilitation were kept constant, abrupt increases in AV nodal activation rate caused a slow (tau = 75 beats) increase in AH interval (fatigue). Vagal stimulation increased the magnitude of this process (maximum: control, 11 +/- 2 msec; vagus, 27 +/- 3 msec; p less than 0.001), without altering its time course. At activation rates comparable to sinus rhythm in humans, vagal stimulation at an intermediate voltage increased the AH interval by 25 msec. As heart rate increased, vagally induced changes in dynamic processes amplified AH prolongation up to fivefold at maximum rate. The role of vagal changes in individual functional properties depended on heart rate, but slowing of recovery was the single most important factor, constituting over 50% of overall vagal action at rapid rates. We conclude that vagal stimulation alters the ways in which the AV node responds to changes in activation rate and that at rapid rates most of the negative dromotropic action of the vagus is due to changes in the AV nodal response to tachycardia. Alterations in rate-dependent AV nodal properties are a novel and potentially important mechanism through which interventions may affect AV nodal conduction.

Animals↗