Excess tachycardia: heart rate after antimuscarinic agents in conscious dogs

Rigel, Dean F.; Lipson, D.; Katona, P. G.

doi:10.1152/ajpheart.1984.246.2.h168

Cited by 29 publications

(15 citation statements)

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“…It was assumed that the HR after atropine was similar to that after vagotomy or vagal cooling. However, an extra component of tachycardia beyond that directly attributable to muscarinic blockade has been observed in the dog after atropine [51]. It is important in the context of this review to mention that this excess tachycardia is not mediated by the beta‐adrenergic system.…”

Section: Sympathetic Control Of Hrvmentioning

confidence: 99%

Sympathetic control of short‐term heart rate variability and its pharmacological modulation

Elghozi

Julien

2007

Fundamemntal Clinical Pharma

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In a broad sense, any change in heart rate (HR) qualifies as HR variability (HRV). As the mechanism of these changes can differ widely, it is relevant to categorize them. Seven types have been proposed. From slowest to fastest: (i) age-related changes [1,2]; (ii) seasonal changes [3]; (iii) circadian or daily rhythms reflecting alterations in autonomic nervous activity throughout the day-night cycle [4], and HRV is, as expected, reduced in autonomic failure [5]; (iv) hourly rhythms (3-, 4-, or 6-h period lengths): these rhythms can be considered submultiples of the circadian rhythm; (v) minute changes (0.5-to 5-min-period lengths or 0.003 to 0.03 Hz): these HR changes are also called very-lowfrequency (VLF) fluctuations. Reductions of VLF RR interval fluctuations are associated with increased risk of cardiac and arrhythmic death [6] and possibly syncope [7,8]. Physical activity influences this HRV component [9]. The renin-angiotensin-aldosterone system also contributes to these fluctuations, through fluctuations in blood pressure [10,11] A B S T R A C TThe static relationship between heart rate (HR) and the activity of either vagal or sympathetic nerves is roughly linear within the physiological range of HR variations. The dynamic control of HR by autonomic nerves is characterized by a fixed time delay between the onset of changes in nerve activity and the onset of changes in HR. This delay is much longer for sympathetically than for vagally mediated changes in HR. In addition, the kinetics of the HR responses shows the properties of a low-pass filter with short (vagal) and long (sympathetic) time constants. These differences might be secondary to differences in nervous conduction times, width of synaptic cleft, kinetics of receptor activation and post-receptor events. Because of the accentuated low-pass filter characteristics of the HR response to sympathetic modulation, sympathetic influences are almost restricted to the very-low-frequency component of HR variability, but the chronotropic effects of vagal stimulation usually predominate over those of sympathetic stimulation in this frequency band. Oscillations in cardiac sympathetic nerve activity are not involved in respiratory sinus arrhythmia (highfrequency component) and make a minor contribution to HR oscillations of approximately 10-s period (low-frequency component of approximately 0.1 Hz), at least in the supine position. In the latter case, HR oscillations are derived mainly from a baroreflex, vagally mediated response to blood pressure Mayer waves. Beta-blockers and centrally acting sympathoinhibitory drugs share the ability to improve the baroreflex control of HR, possibly through vagal facilitation, which might be beneficial in several cardiovascular diseases.

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Section: Sympathetic Control Of Hrvmentioning

confidence: 99%

Sympathetic control of short‐term heart rate variability and its pharmacological modulation

Elghozi

Julien

2007

Fundamemntal Clinical Pharma

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“…4). This phenomenon probably corresponds to 'excess tachyeardia', which occurs with strong vagal activation during cholinergic block alone, and more clearly with cholinergic and ,-adrenergic block (Rigel, Lipson & Katona, 1984). Strong vagal activation would have occurred in our experiments when carotid sinus pressure was increased to high levels.…”

Section: Mechanism Of Veratrine's Effect On the Baroreflexmentioning

confidence: 59%

“…Strong vagal activation would have occurred in our experiments when carotid sinus pressure was increased to high levels. Excess tachycardia may be caused by the release (from preganglionic or postganglionic parasympathetic neurons) of a neurotransmitter that has a cardioacceleratory action (Rigel et al 1984).…”

Section: Mechanism Of Veratrine's Effect On the Baroreflexmentioning

confidence: 99%

Intracoronary veratrine attenuates carotid baroreceptor reflex regulation of blood pressure in conscious dogs.

Denison

Stephenson

Hull

et al. 1992

The Journal of Physiology

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SUMMARY1. The effect of activation of left ventricular cardiac receptors on carotid baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance was determined in conscious dogs. Previous studies in conscious subjects assessed only the effect on baroreflex control of heart rate.2. Dogs with denervated aortic baroreceptors were equipped with aortic flow probes, cardiac pacing electrodes, and catheters in the aorta, vena cava, and left circumflex coronary artery. Both carotid sinus regions were prepared for reversible vascular isolation.3. Left ventricular receptors were stimulated by an infusion of veratrine (0-1-1P0 gug kg-' min-') into the left circumflex coronary artery. 4. Veratrine infusion decreased control blood pressure only 10+2 mmHg, but it decreased the range of baroreflex control of blood pressure by 50% and decreased maximum baroreflex gain by 42 %. Both the cardiac output and total peripheral resistance components of the baroreflex were attenuated.5. Baroreflex control of blood pressure was unaffected by intravenous veratrine or by intracoronary infusion of vehicle.6. Intracoronary veratrine had no effect after autonomic ganglionic blockade. 7. When cardiac output was kept nearly constant (by ,-adrenergic and cholinergic receptor blockade or by fl-blockade and cardiac pacing), intracoronary veratrine still attenuated baroreflex control of blood pressure and total peripheral resistance. Veratrine impaired the ability of the baroreflex to utilize cz-adrenergic mechanisms to control total peripheral resistance.8. We conclude that activation of ventricular receptors attenuates baroreflex regulation of blood pressure in conscious dogs through an attenuation of baroreflex control of both cardiac output and total peripheral resistance.

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“…Many studies attempted to explain the phenomenon of "excess tachycardia," where the heart rate is the presence of muscarinic blockade exceeds the heart rate due to ganglionic blockade (Bmnsting et al 1979(Bmnsting et al , 1983Schuil et al 198 1 ;Rigel et al 1984Rigel et al , 1986 and exceeds the heart rate following the transsection or cooling of both vagi (Rudnicki et d. 199 1). Although the receptors and neurotransmitters are not hlly understood, the involvement of antihistaminic agents, local anesthetics, and peptide neurotransmitters was demonstrated by Rigel et al (Rigel 1988;Rigel et al 1989Rigel et al , 1990Rigel et al , 1991.…”

Section: D~s E Of Aratirnuscarinic Agent (X Initial Dose)mentioning

confidence: 99%

Muscarinic and ganglionic blocking properties of atropine compounds in vivo and in vitro: time dependence and heart rate effects

Vicenzi

Woehick²,

Boban³

et al. 1995

Can. J. Physiol. Pharmacol.

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High doses (3 mg/kg) of methylatropine nitrate have been used in vivo to produce long-lasting muscarinic blockade during physiologic experiments. At these levels, the possibility exists that ganglionic blockade may also be responsible for some heart rate effects. Therefore, the effects of methylatropine nitrate (0.0012-2.4 mg.kg(-1)) and atropine sulfate (0.0036 - 0.060 mg.kg(1)) were evaluated in vivo using conscious dogs and in vitro using canine right atria and isolated stellate ganglia. The lowest doses of either agent given in vivo caused bradycardia, while intermediate doses induced excess tachycardia. High doses of methylatropine nitrate transiently decreased the heart rate, followed by slow recovery. In vitro using the canine right atria, neither drug caused pacemaker shifts nor directly altered the atrial rate, but postvagal tachycardia occurred with acetylcholine challenge and was prevented by metoprolol or 6-hydroxydopamine. In vitro studies using the canine stellate ganglia indicate that both agents depressed postganglionic compound action potentials at high doses. In conclusion, with high-dose methylatropine nitrate, ganglionic blockade yields the mechanism for a reduction of excess tachycardia as well as a likely explanation for opposing chronotropic effects in conscious and anesthetized dogs. In experimental studies where high doses of atropine compounds are used for long-term muscarinic blockade, it is possible that ganglionic blocking effects may also be produced.

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Excess tachycardia: heart rate after antimuscarinic agents in conscious dogs

Cited by 29 publications

References 0 publications

Sympathetic control of short‐term heart rate variability and its pharmacological modulation

Sympathetic control of short‐term heart rate variability and its pharmacological modulation

Intracoronary veratrine attenuates carotid baroreceptor reflex regulation of blood pressure in conscious dogs.

Muscarinic and ganglionic blocking properties of atropine compounds in vivo and in vitro: time dependence and heart rate effects

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