Heart rate responses to a muscarinic agonist in rats with experimentally induced acute and subacute chagasic myocarditis

We administered arecoline to rats, with experimentally induced chagasic myocarditis, in order to study the sinus node sensitivity to a muscarinic agonist. Sixteen month old rats were inoculated with 200,000 T. cruzi parasites ("Y" strain). Between days 18 and 21 (acute stage), 8 infected rats and 8 age-matched controls received intravenous arecoline as a bolus injection at the following doses: 5.0, 10.0, 20.0, 40.0, and 80.0 mug/kg. Heart rate was recorded before, during and after each dose of arecoline. The remaining 8 infected animals and 8 controls were subjected to the same experimental procedure during the subacute stage, i.e., days 60 to 70 after inoculation. The baseline heart rate, of the animals studied during the acute stage (349 ± 68 bpm, mean ± SD), was higher than that of the controls (250 ± 50 bpm, p < 0.005). The heart rate changes were expressed as percentage changes over baseline values. A dose-response curve was constructed for each group of animals. Log scales were used to plot the systematically doubled doses of arecoline and the induced-heart rate changes. The slope of the regression line for the acutely infected animals (r = - 0.99, b =1.78) was not different from that for the control animals (r = - 0.97, b = 1.61). The infected animals studied during the subacute stage (r = - 0.99, b = 1.81) were also not different from the age-matched controls (r = - 0.99, b = 1.26, NS). Consequently, our results show no pharmacological evidence of postjunctional hypersensitivity to the muscarinic agonist arecoline. Therefore, these results indirectly suggest that the postganglionic parasympathetic innervation, of the sinus node of rats with autopsy proved chagasic myocarditis, is not irreversibly damaged by Trypanosoma cruzi.

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Cardiac sympathetic-parasympathetic balance in rats with experimentally-induced acute chagasic myocarditis

Revista do Instituto de Medicina Tropical de São Paulo ◽

10.1590/s0036-46651995000200011 ◽

1995 ◽

Vol 37 (2) ◽

pp. 155-159 ◽

Cited By ~ 11

Author(s):

Diego F. Davila ◽

Carlos F. Gotterberg ◽

Argenis Torres ◽

Geza Holzhaker ◽

Richard Barrios ◽

...

Keyword(s):

Heart Rate ◽

Beta Blocker ◽

Sympathetic Activity ◽

Sinus Tachycardia ◽

Acute Stage ◽

Baseline Heart Rate ◽

Cardiac Sympathetic Activity ◽

Chronotropic Response ◽

Cardiac Parasympathetic Activity ◽

Experimentally Induced

To clarify the mechanism responsible for the transient sinus tachycardia in rats with acute chagasic myocarditis, we have examined the cardiac sympathetic-parasympathetic balance of 29 rats inoculated with 200,000 parasites (Trypanosoma cruzi). Sixteen infected animals and 8 controls were studied between days 18 and 21 after inoculation (acute stage). The remaining 13 infected animals and 9 controls were studied between days 60 and 70 after inoculation (sub-acute stage). Under anesthesia (urethane 1.25 g/kg), all animals received intravenous atenolol (5 mg/kg) and atropine (10 mg/kg). Acute stage: The baseline heart rate of the infected animals was significantly higher than that of the controls (P < 0.0001). The magnitude of the negative chronotropic response to atenolol was 4 times that of the controls (P < 0.00001). This response correlated with the baseline heart rate (r= - 0.72, P < 0.001). The heart rate responses to the beta-blocker and to atropine, of the infected animals studied during the sub-acute stage, were not different from controls. These findings suggest that cardiac sympathetic activity is transiently enhanced and cardiac parasympathetic activity is not impaired, in rats with acute chagasic myocarditis. The transient predominance of cardiac sympathetic activity could explain, in part, the sinus tachycardia observed in the acute stage of experimentally-induced chagasic myocarditis.

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P1097Heart rate acceleration is a poor surrogate of complete parasympathetic denervation of sinus node during cardioneuroablation

EP Europace ◽

10.1093/europace/euaa162.044 ◽

2020 ◽

Vol 22 (Supplement_1) ◽

Author(s):

D Wichterle ◽

H Jansova ◽

P Stiavnicky ◽

P Peichl ◽

R Cihak ◽

...

Keyword(s):

Heart Rate ◽

Sinus Rhythm ◽

Nerve Stimulation ◽

Sinus Node ◽

Clinical Success Rate ◽

Vagal Nerve ◽

Vagal Nerve Stimulation ◽

High Frequency Stimulation ◽

Baseline Heart Rate ◽

Rate Acceleration

Abstract Background Ablation of superior paraseptal ganglionic plexi is invariantly associated with the acceleration of sinus rhythm. This is considered a favourable sign during cardioneuroablation for the treatment of recurrent neurally-mediated cardioinhibitory syncope or symptomatic sinus bradycardia. Purpose In this retrospective study, we investigated whether the magnitude of sinus rhythm acceleration corresponds with directly assessed sinus nodal parasympathetic denervation. Methods The study included 48 patients (age: 39 ± 13 years, 58% males) who underwent cardioneuroablation in general anaesthesia. The procedural endpoint was non-responsiveness (i.e. loss of original cardioinhibitory response) of the sinus node to extracardiac high-frequency stimulation of the vagal nerve. The magnitude of sinus rhythm acceleration was compared between patients who reached or did not reach this endpoint. Results All patients had positive atropine test (baseline heart rate: 65 ± 14 bpm; post-atropine: 109 ± 22 bpm). Complete sinus nodal denervation as assessed by vagal nerve stimulation was achieved in 44/48 (92%) patients. Intraprocedurally, heart rate accelerated from 54 ± 11 to 85 ± 14 bpm (difference: 31 ± 10; median 29; interquartile range: 24–40; total range: 13–61 bpm). This change did not correlate with age and was not related to pre-procedural post-atropine sinus rhythm acceleration. There was no difference in heart rate acceleration between the patient with and without sinus nodal denervation (Figure). Conclusions Sinus rhythm acceleration is not reliable endpoint for cardioneuroablation. Guidance by extracardiac vagal nerve stimulation may help to tailor the procedures to increase the clinical success rate and, at the same time, to avoid patient overtreatment. Abstract Figure.

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814 Influence of sinus node dysfunction, diabetes mellitus and surgical heart denervation on heart rate turbulence

EP Europace ◽

10.1016/s1099-5129(05)80554-9 ◽

2005 ◽

Vol 7 ◽

pp. 188-188

Keyword(s):

Diabetes Mellitus ◽

Heart Rate ◽

Sinus Node ◽

Sinus Node Dysfunction ◽

Heart Rate Turbulence

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RNAseq shows an all-pervasive day-night rhythm in the transcriptome of the pacemaker of the heart

Scientific Reports ◽

10.1038/s41598-021-82202-7 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Yanwen Wang ◽

Cali Anderson ◽

Halina Dobrzynski ◽

George Hart ◽

Alicia D’Souza ◽

...

Keyword(s):

Heart Rate ◽

Nervous System ◽

Circadian Clock ◽

Sick Sinus Syndrome ◽

Sinus Node ◽

Signalling Pathways ◽

Resting Heart Rate ◽

Ion Channel Regulation ◽

Channel Regulation ◽

Physiological Systems

AbstractPhysiological systems vary in a day-night manner anticipating increased demand at a particular time. Heart is no exception. Cardiac output is primarily determined by heart rate and unsurprisingly this varies in a day-night manner and is higher during the day in the human (anticipating increased day-time demand). Although this is attributed to a day-night rhythm in post-translational ion channel regulation in the heart’s pacemaker, the sinus node, by the autonomic nervous system, we investigated whether there is a day-night rhythm in transcription. RNAseq revealed that ~ 44% of the sinus node transcriptome (7134 of 16,387 transcripts) has a significant day-night rhythm. The data revealed the oscillating components of an intrinsic circadian clock. Presumably this clock (or perhaps the master circadian clock in the suprachiasmatic nucleus) is responsible for the rhythm observed in the transcriptional machinery, which in turn is responsible for the rhythm observed in the transcriptome. For example, there is a rhythm in transcripts responsible for the two principal pacemaker mechanisms (membrane and Ca2+ clocks), transcripts responsible for receptors and signalling pathways known to control pacemaking, transcripts from genes identified by GWAS as determinants of resting heart rate, and transcripts from genes responsible for familial and acquired sick sinus syndrome.

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Heart rate variability and depressive symptoms: a cross-lagged analysis over a 10-year period in the Whitehall II study

Psychological Medicine ◽

10.1017/s003329171600060x ◽

2016 ◽

Vol 46 (10) ◽

pp. 2121-2131 ◽

Cited By ~ 48

Author(s):

V. K. Jandackova ◽

A. Britton ◽

M. Malik ◽

A. Steptoe

Keyword(s):

Heart Rate ◽

Heart Rate Variability ◽

Depressive Symptoms ◽

General Health Questionnaire ◽

Antidepressant Medication ◽

Population Based ◽

Baseline Heart Rate ◽

Lower Baseline ◽

The Uk

BackgroundPeople with depression tend to have lower heart rate variability (HRV), but the temporal sequence is poorly understood. In a sample of the general population, we prospectively examined whether HRV measures predict subsequent depressive symptoms or whether depressive symptoms predict subsequent levels of HRV.MethodData from the fifth (1997–1999) and ninth (2007–2009) phases of the UK Whitehall II longitudinal population-based cohort study were analysed with an average follow-up of 10.5 years. The sample size for the prospective analysis depended on the analysis and ranged from 2334 (644 women) to 2276 (602 women). HRV measures during 5 min of supine rest were obtained. Depressive symptoms were evaluated by four cognitive symptoms of depression from the General Health Questionnaire.ResultsAt follow-up assessment, depressive symptoms were inversely associated with HRV measures independently of antidepressant medication use in men but not in women. Prospectively, lower baseline heart rate and higher HRV measures were associated with a lower likelihood of incident depressive symptoms at follow-up in men without depressive symptoms at baseline. Similar but statistically insignificant associations were found in women. Adjustments for known confounders including sociodemographic and lifestyle factors, cardiometabolic conditions or medication did not change the predictive effect of HRV on incident depressive symptoms at follow-up. Depressive symptoms at baseline were not associated with heart rate or HRV at follow-up in either sex.ConclusionsThese findings are consistent with an aetiological role of the autonomic nervous system in depression onset.

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Anabolic-androgenic steroids: Effects on social behavior and baseline heart rate.

Health Psychology ◽

10.1037/0278-6133.9.6.774 ◽

1990 ◽

Vol 9 (6) ◽

pp. 774-791 ◽

Cited By ~ 13

Author(s):

W. Jack Rejeski ◽

Edward Gregg ◽

Jay R. Kaplan ◽

Stephen B. Manuck

Keyword(s):

Heart Rate ◽

Social Behavior ◽

Anabolic Androgenic Steroids ◽

Baseline Heart Rate ◽

Androgenic Steroids

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Baseline heart rate variability (HRV) and performance during a set-shifting visuospatial learning task: the moderating effect of trait negative affectivity (NA) on behavioral flexibility

Physiology & Behavior ◽

10.1016/j.physbeh.2021.113647 ◽

2021 ◽

pp. 113647

Author(s):

Breannan C. Howell ◽

Derek A. Hamilton

Keyword(s):

Heart Rate ◽

Heart Rate Variability ◽

Negative Affectivity ◽

Behavioral Flexibility ◽

Learning Task ◽

Moderating Effect ◽

Baseline Heart Rate ◽

Set Shifting ◽

Visuospatial Learning ◽

And Performance

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Abstract 2140: Infrequent Need for Pacing Following Implantable Cardioverter-Defibrillator Shocks: Analysis of the Sudden Cardiac Death in Heart Failure Trial

Circulation ◽

10.1161/circ.118.suppl_18.s_674 ◽

2008 ◽

Vol 118 (suppl_18) ◽

Author(s):

Jordan M Prutkin ◽

Jeanne E Poole ◽

George Johnson ◽

Jill Anderson ◽

Daniel B Mark ◽

...

Keyword(s):

Heart Failure ◽

Heart Rate ◽

Sudden Cardiac Death ◽

Cardiac Death ◽

Nyha Class ◽

Prior History ◽

Baseline Heart Rate ◽

Implantable Cardioverter Defibrillators ◽

Heart Failure Trial ◽

Post Shock

Background: Implantable cardioverter-defibrillators (ICD) are routinely programmed to pace after a shock to prevent possible asystole. In those with no prior history of bradycardia, there is little data regarding the prevalence and characteristics of those who use post-shock pacing (PSP). Methods: We analyzed the occurrence of pacing within the first nine beats after the first successful ICD shock for ventricular tachycardia (VT) or ventricular fibrillation (VF) in the Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT). All ICDs were single lead with the first PSP delivered at 1400msec and all subsequent stimuli delivered at 1200msec. We excluded patients with pacing during pre-shock rhythms and those who had pacing rates different than the protocol default rate of 50bpm (1200 msec). Results: There were 2521 patients enrolled in SCD-HeFT, of which 811 received an ICD. A total of 153 shock events were examined; 36 (23.5%) had at least one of the first nine beats paced post-shock, though only 4 (2.5%) had greater than 4 out of the 9 beats paced. No subjects needed pacing for all nine beats and only 8 (5.2%) paced for greater than 5 seconds. There were no differences in age, gender, etiology of cardiomyopathy, or NYHA class between those with PSP or not. The prevailing heart rate pre-shock was predictive of PSP; the mean cycle length of the baseline rhythm pre-shock was longer (slower rate) for those who used PSP (735 ± 228msec vs. 624 ± 158msec, P=0.001). More often, VF (vs. VT) was the rhythm shocked in those using PSP (P=0.015). A trend also was seen toward increased frequency of PSP in those receiving 30J shocks (16 of 49) versus ≤20J shocks (20 of 104, P=0.068). Conclusion: Patients infrequently require multiple paced beats post-shock for VT or VF. Patients using PSP have a slower baseline heart rate and are more likely to have VF as the shocked rhythm. While 1 or 2 paced beats out of the first nine occurred occasionally, these patients also had rapid return of their native rhythm for which the hemodynamic contribution of 1 or 2 paced beats is unclear. These data suggest that for most patients receiving a primary prevention ICD programmed for shock-only therapy, the need for PSP is limited. PSP use may reflect convention and the assumption that minor post-shock pauses are detrimental.

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Cardiac enkephalins attenuate vagal bradycardia: interactions with NOS-1-cGMP systems in canine sinoatrial node

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00275.2003 ◽

2003 ◽

Vol 285 (5) ◽

pp. H2001-H2012 ◽

Cited By ~ 10

Author(s):

Martin Farias ◽

Keith Jackson ◽

Michael Johnson ◽

James L. Caffrey

Keyword(s):

Heart Rate ◽

Phosphodiesterase Inhibitor ◽

Endogenous Opioids ◽

Muscarinic Agonist ◽

No Donor ◽

Parasympathetic Nerve ◽

Sa Node ◽

Vagal Control ◽

Nos Inhibitors ◽

Vagal Bradycardia

Endogenous opioids and nitric oxide (NO) are recognized modulators of cardiac function. Enkephalins and inhibitors of NO synthase (NOS) both produce similar interruptions in the vagal control of heart rate. This study was conducted to test the hypothesis that NO systems within the canine sinoatrial (SA) node facilitate local vagal transmission and that the endogenous enkephalin methionine-enkephalin-arginine-phenylalanine (MEAP) attenuates vagal bradycardia by interrupting the NOS-cGMP pathway. Microdialysis probes were inserted into the SA node, and they were perfused with nonselective ( Nω-nitro-l-arginine methyl ester) and neuronal (7-nitroindazole) NOS inhibitors. The right vagus nerve was stimulated and both inhibitors gradually attenuated the resulting vagal bradycardia. The specificity of these inhibitions was verified by an equally gradual reversal of the inhibition with an excess of the NOS substrate l-arginine. Introduction of MEAP into the nodal interstitium produced a quickly developing but quantitatively similar interruption of vagal bradycardia that was also slowly reversed by the addition of l-arginine and not by d-arginine. Additional support for convergence of opioid and NO pathways was provided when the vagolytic effects of MEAP were also reversed by the addition of the NO donor S-nitroso- N-acetyl-penicillamine, the protein kinase G activator 8-bromo-cGMP, or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine. MEAP and 7-nitroindazole were individually combined with the direct acting muscarinic agonist methacholine to evaluate potential interactions with muscarinic receptors within the SA node. MEAP and 7-nitroindazole were unable to overcome the bradycardia produced by methacholine. These data suggest that NO and enkephalins moderate the vagal control of heart rate via interaction with converging systems that involve the regulation of cAMP within nodal parasympathetic nerve terminals.

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