The influence of acute sympathetic denervation, reserpine and choline xylyl ether on vagal escape

Campos, H. A.; Friedman, Alexander H.

doi:10.1113/jphysiol.1963.sp007254

Cited by 12 publications

(6 citation statements)

References 22 publications

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“…All these findings suggest that a mechanism of this sort might be involved, in the absence of atropine, in the phenomenon of vagal escape. Evidence in favour of this assumption has been presented previously (Friedman & Campos, 1960;Roberts & Stadter, 1960;Campos & Friedman, 1963). In the present work it is shown that cocaine significantly enhances the recovery of the heart from the inhibitory action of the vagus, which is in agreement with recent findings by Moore (1967) in the open-chest dog.…”

Section: Discussionsupporting

confidence: 93%

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Action of cocaine and chronic sympathetic denervation on vagal escape

Campos¹,

Urquilla²

1969

The Journal of Physiology

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SUMMARY1. The effect of cocaine has been studied on vagal escape and on the tachycardia due to vagal stimulation in the atropinized dog. All 4. Chronic thoracic sympathectomy markedly retards the recovery of the ventricular rate from the inhibitory action of the vagus. Under this condition, the infusion of cocaine does not significantly enhance the ventricular escape.5. These findings suggest that an adrenergic mechanism located at the sympathetic nerves supplying the heart is substantially involved in the phenomenon of vagal escape.

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Section: Discussionsupporting

confidence: 93%

“…Conversely a retardation of the escape pattern was indicated by a decrease in this value in comparison with the control. In order to facilitate comparison of the effects of treatments, means of the final cumulative percentage values were expressed as percentages of untreated control group values (Campos & Friedman. 1963).…”

Section: Introductionmentioning

confidence: 99%

Action of cocaine and chronic sympathetic denervation on vagal escape

Campos¹,

Urquilla²

1969

The Journal of Physiology

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“…At the organ level, excess vagal nerve stimulation eventually causes cardiac asystole, followed by resumption of the heartbeat. This desensitization is called vagal escape and has been explained by compensation from the sympathetic system (17)(18)(19)(20). Although ACh causes short-term desensitization of I KACh and vagal escape, the functional relevance of these two different phenomena has not been previously examined.…”

Section: Introductionmentioning

confidence: 99%

Short-Term Desensitization of Muscarinic K+ Current in the Heart

Murakami

Inanobe

Kurachi

2013

Biophysical Journal

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Acetylcholine (ACh) rapidly increases cardiac K(+) currents (IKACh) by activating muscarinic K(+) (KACh) channels followed by a gradual amplitude decrease within seconds. This phenomenon is called short-term desensitization and its precise mechanism and physiological role are still unclear. We constructed a mathematical model for IKACh to examine the conditions required to reconstitute short-term desensitization. Two conditions were crucial: two distinct muscarinic receptors (m2Rs) with different affinities for ACh, which conferred an IKACh response over a wide range of ACh concentrations, and two distinct KACh channels with different affinities for the G-protein βγ subunits, which contributed to reconstitution of the temporal behavior of IKACh. Under these conditions, the model quantitatively reproduced several unique properties of short-term desensitization observed in myocytes: 1), the peak and quasi-steady states with 0.01-100 μM [ACh]; 2), effects of ACh preperfusion; and 3), recovery from short-term desensitization. In the presence of 10 μM ACh, the IKACh model conferred recurring spontaneous firing after asystole of 8.9 s and 10.7 s for the Demir and Kurata sinoatrial node models, respectively. Therefore, two different populations of KACh channels and m2Rs may participate in short-term desensitization of IKACh in native myocytes, and may be responsible for vagal escape at nodal cells.

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“…The latter is commonly referred to as " vagal escape " (Bard, 1956a). Although the mechanism of the escape phenomenon is unresolved, evidence has accumulated which indicates that adrenergic factors may be involved, possibly through a local release of catecholamines by acetylcholine (Campos & Freidman, 1963;Moore, 1967).To evaluate the local release hypothesis, the effects of beta adrenergic and postganglionic parasympathetic blockade on the chronotropic action of the vagus were determined in this study. In the course of our experiments, interesting data were obtained on the effect of stimulation frequency on the duration of vagally induced cardiac asystole and the intracardiac origin of the ensuing vagal escape.…”

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confidence: 99%

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confidence: 99%

Cardiac Effects of Vagal Stimulation in the Anaesthetized Cat

Miller¹,

Pendleton²,

Richmond³

1968

British Journal of Pharmacology and Chemotherapy

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Continuous stimulation of the right vagus nerve in anaesthetized animals can produce cardiac asystole, followed by a reinitiation of the heart beat. The latter is commonly referred to as " vagal escape " (Bard, 1956a). Although the mechanism of the escape phenomenon is unresolved, evidence has accumulated which indicates that adrenergic factors may be involved, possibly through a local release of catecholamines by acetylcholine (Campos & Freidman, 1963;Moore, 1967).To evaluate the local release hypothesis, the effects of beta adrenergic and postganglionic parasympathetic blockade on the chronotropic action of the vagus were determined in this study. In the course of our experiments, interesting data were obtained on the effect of stimulation frequency on the duration of vagally induced cardiac asystole and the intracardiac origin of the ensuing vagal escape. The cat was used in all experiments because the vagus and cervical sympathetic nerves can be easily separated in this species (Liddell & Sherrington, 1929). METHODSCats of either sex, weighing between 2 and 5 kg, were anaesthetized intraperitoneally with a-chloralose, 85 mg/kg, and placed on a heated cat board. A tracheotomy was performed, and the exposed part of the cannula was covered with non-conducting electrical tape. Arterial blood pressure was recorded from the right femoral artery with a cannula leading to a Statham P 23 Db transducer and Sanborn Model 296 recorder. The right femoral vein was cannulated for injection of drug solutions. The Lead II electrocardiogram was recorded from subcutaneous needle electrodes with a Sanborn Model 100 Viso-Cardiette recorder. The left vagosympathetic trunk was isolated and cut. The corresponding right trunk was isolated, the cervical sympathetic section was isolated and severed, and the vagus was tied with suture and crushed central to the tie. Throughout the experiments, the right vagus was kept warm (-37' C) and moist with Locke-Ringer solution.The vagus was stimulated with bipolar platinum electrodes leading from American Electronics Laboratory stimulus isolation and stimulator units. Supramaximal voltage was determined for each preparation by selecting the voltage required to produce a maximal slowing of the heart rate at a stimulation frequency of 5 c/s.

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The influence of acute sympathetic denervation, reserpine and choline xylyl ether on vagal escape

Cited by 12 publications

References 22 publications

Action of cocaine and chronic sympathetic denervation on vagal escape

Action of cocaine and chronic sympathetic denervation on vagal escape

Short-Term Desensitization of Muscarinic K+ Current in the Heart

Cardiac Effects of Vagal Stimulation in the Anaesthetized Cat

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