Effect of Enhanced Contractility on the Left Ventricular Response to Vagus Nerve Stimulation in Dogs

Levy, Matthew N.; Zieske, Harrison

doi:10.1161/01.res.24.3.303

Cited by 55 publications

(31 citation statements)

References 23 publications

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“…The positive inotropic action of phenylephrine was also antagonized prominently by the same concentration of carbachol. The accentuated antagonism on the mammalian ventricular myocardium (16), as described usually for whole animal experiments (11)(12)(13)(14)(15) as well as in the isolated ventricular muscle (17), was confirmed to be operative also in the canine isolated ventricular muscle.…”

Section: Discussionmentioning

confidence: 80%

Failure of dibutyryl and 8-bromo-cyclic gmp to mimic the antagonistic action of carbachol on the positive inotropic effects of sympathomimetic amines in the canine isolated ventricular myocardium

Endoh

Shimizu

1979

Japanese Journal of Pharmacology

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Abstract-Effects of carbachol, dbcGMP and 8-bromo-cyclic GMP on the positive inotropic actions of sympathomimetic amines and dbcAMP were studied on the canine isolated right ventricular myocardium.Carbachol alone did not substantially change the developed tension of the muscle, but did markedly shift the dose response curve for isoprenaline on the developed tension to the right and depressed the maximal response to the drug in a concentration dependent manner. The positive inotropic action of phenylephrine was affected by carbachol in the same manner as that of isoprenaline. DbcGMP in concentrations of 10-3 M and higher produced a significant increase in the developed tension. The positive inotropic action of dbcGMP was partly inhibited by a Q-adrenoceptor blocking agent, pindolol. In the presence of dbcGMP, isoprenaline produced an action similar to that seen in the control experiment, but this action was not maintained on such a steady level as in the control.This rapid decline of the effect of isoprenaline in the presence of dbcGMP was prevented by adding ascorbic acid to the organ bath. The positive inotropic actions of phenylephrine and of dbcAMP were not substantially affected by dbcGMP.8-Bromo-cyclic GMP in a concentration of 10-' M did not change either the basal developed tension or the positive inotropic actions of noradrenaline and of isoprenaline.The present results indicate that these cyclic GMP derivatives are not able to mimic the antagonistic action of cholinergic stimulation on the positive inotropic action of adrenergic stimulation on the canine ventricular myocardium.

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Section: Discussionmentioning

confidence: 80%

Failure of dibutyryl and 8-bromo-cyclic gmp to mimic the antagonistic action of carbachol on the positive inotropic effects of sympathomimetic amines in the canine isolated ventricular myocardium

Endoh

Shimizu

1979

Japanese Journal of Pharmacology

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“…It is well known that there may be significant sympathetic-parasympathetic interactions. These interactions may result in enhanced parasympathetic effects (17,22) during exercise and/or recovery, a phenomenon termed "accentuated antagonism" (17,19,20,25). Nevertheless, the physiology of interest is the parasympathetic effect that is noted during exercise and recovery, when there is enhanced sympathetic tone.…”

Section: Discussionmentioning

confidence: 99%

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Kannankeril

Goldberger

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Depressed parasympathetic tone is associated with an increased risk of sudden cardiac death. Exercise and the postexercise recovery period, which are associated with parasympathetic withdrawal, are high risk periods for sudden death. However, parasympathetic effects on cardiac electrophysiology during exercise and recovery have not been described. Electrophysiology studies were performed using noninvasive programmed stimulation (NIPS) in nine subjects (age 59 Ϯ 18 yr) with implanted dual-chamber devices and normal left ventricular function during multiple bicycle exercise sessions. NIPS was performed at rest, during exercise, and in the early recovery period both before and after parasympathetic blockade with atropine. Parasympathetic effect was defined as the value of the parameter of interest in the absence of atropine minus the value of the parameter in the presence of atropine. During exercise, sinus cycle length, atrioventricular (AV) block cycle length, AV interval, and ventricular effective refractory period shortened; in recovery, the values were intermediate between the rest and exercise values (P Ͻ 0.0001 by ANOVA). Parasympathetic effects on sinus cycle length, AV block cycle length, AV interval, and ventricular effective refractory period were 247 Ϯ 140, 58 Ϯ 20, 76 Ϯ 20, and 8.6 Ϯ 7.5 ms at rest, 106 Ϯ 20, 37 Ϯ 14, 24 Ϯ 13, and 2.6 Ϯ 7.8 ms during exercise, and 209 Ϯ 114, 50 Ϯ 23, 35 Ϯ 21, and 9.5 Ϯ 11.8 ms during recovery, respectively. There was poor correlation among the parasympathetic effects noted at the sinus node, AV node, and ventricle. Further work evaluating parasympathetic effects on cardiac electrophysiology during exercise and recovery in patients with heart disease is required to elucidate its role in modulating the risk of sudden cardiac death noted at these times. exercise THE RISK OF SUDDEN DEATH is increased nearly 17-fold during and immediately after exercise (2, 23). While there are several potential mechanisms for this marked increased risk of sudden cardiac death, it is possibly related in part to the acute changes in autonomic tone that accompany exercise. Exercise is associated with increased sympathetic tone and parasympathetic withdrawal in normal subjects (11,12,36).Numerous clinical and experimental studies have provided evidence linking diminished parasympathetic nervous system activity at rest with increased mortality and sudden cardiac death (6,16,18,28,31). Experimental data suggest that dogs with myocardial infarctions prone to ventricular fibrillation during exercise and induced ischemia have greater reductions in parasympathetic tone, as measured by heart rate variability, during exercise compared with nonsusceptible animals (7). Recent human data have shown that a small heart rate decrease in the early recovery phase after exercise is associated with an increased mortality (9,10,27). These data suggest that depressed parasympathetic tone during exercise or depressed recovery of parasympathetic tone after exercise may be important factors resulting in an increased...

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“…24 Vagal antagonistic action, by opposing sympathetic actions at both pre-and postjunctional levels, 25,26 exists not only in the chronotropic effect but also in the control of ventricular performance, intracellular calcium handling, and cardiac electrophysiology. 4,27,28 Schwartz et al 29 demonstrated in chloralose anesthetized cats that afferent vagus nerve stimulation (VNS) reflexively inhibited efferent sympathetic nerve activity. About 40 years later, using an implanted device to record autonomic nerve activity continuously in ambulatory canines, Shen et al 30 observed that chronic left-sided cervical VNS led to a significant reduction in sympathetic nerve activity from the left stellate ganglion (LSG).…”

Section: Autonomic Influences On Cardiac Electrophysiology Interplay mentioning

confidence: 99%

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

Shen

Zipes

2014

Circulation Research

677

543

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I n 1628, William Harvey hinted at a link between the brain and the heart when he wrote, "For every affection of the mind that is attended with either pain or pleasure, hope or fear, is the cause of an agitation whose influence extends to the heart."1 For the past half century, numerous anatomic and physiological studies of cardiac autonomic nervous system (ANS) 2-6 have investigated this link and found it to be very complex. Autonomic activation alters not only heart rate, conduction, and hemodynamics, but also cellular and subcellular properties of individual myocytes. The characterization of extrinsic cardiac ANS and intrinsic cardiac ANS ranges from the recognition of anatomic relationships at the gross level to discovery of chemoreceptors, mechanoreceptors, and intracardiac ganglia lining specific regions along the cardiac chambers and great vessels. Moreover, studies beginning >80 years ago [7][8][9] have demonstrated the critical role of cardiac ANS in cardiac arrhythmogenesis. This topic has garnered much recent interest because of mounting evidence showing that neural modulation either by ablation or stimulation can effectively control a wide spectrum of cardiac arrhythmias. [10][11][12][13] In this review, we will briefly discuss the anatomic aspects of cardiac ANS, focusing on how autonomic activities influence cardiac electrophysiology. We will also discuss specific autonomic triggers of various cardiac arrhythmias, including atrial fibrillation (AF), ventricular arrhythmias, and inherited arrhythmia syndromes. Lastly, we will discuss the latest avenues of research and clinical trials regarding the application of neural modulation in the treatment of specific cardiac arrhythmias.

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Effect of Enhanced Contractility on the Left Ventricular Response to Vagus Nerve Stimulation in Dogs

Cited by 55 publications

References 23 publications

Failure of dibutyryl and 8-bromo-cyclic gmp to mimic the antagonistic action of carbachol on the positive inotropic effects of sympathomimetic amines in the canine isolated ventricular myocardium

Failure of dibutyryl and 8-bromo-cyclic gmp to mimic the antagonistic action of carbachol on the positive inotropic effects of sympathomimetic amines in the canine isolated ventricular myocardium

Parasympathetic effects on cardiac electrophysiology during exercise and recovery

Role of the Autonomic Nervous System in Modulating Cardiac Arrhythmias

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