The Action of Cardiac Glycosides on Autonomic Ganglia

Perry, W. L. M.; Reinert, H.

doi:10.1111/j.1476-5381.1954.tb01687.x

Cited by 16 publications

(8 citation statements)

References 11 publications

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“…The attenuated response of the ventricular myocardium to vagal stimulation after acetylstrophanthidin in the present study is the reverse of the phenomenon observed at the cardiac pacemaker, where the response to vagal stimulation is potentiated by the cardiac glycosides (25)(26)(27)(28). Evidently, different mechanisms are involved in the cholinergic interactions with acetylstrophanthidin at the pacemaker and myocardial cells.…”

Section: Levy Zieskesupporting

confidence: 45%

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

Levy

Zieske²

1969

Circulation Research

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In the canine isovolumetric left ventricle preparation, stimuli were applied to the efferent end of a transected cervical vagus nerve. The changes in left ventricular systolic pressure in response to vagal stimulation were compared under control conditions and when ventricular contractility was enhanced by various kinds of inotropic stimulation-left stellate ganglion stimulation, paired pacing, calcium chloride infusions, aminophylline infusions, and acetylstrophanthidin injections. Vagal stimulation under control conditions caused mean decreases in pressure in the various groups ranging from 13.2 to 16.2% of the control level. The depressant effect of vagal stimulation was potentiated during sympathetic stimulation, in confirmation of previous findings; the mean decrease in pressure produced by vagal stimulation during concurrent sympathetic stimulation varied from 20.1 to 20.8%. Calcium and aminophylline infusions had no significant effect on the ventricular response to vagal stimulation; the percent reductions in pressure caused by vagal stimulation were 18.1 and 15.5%, respectively. However, the response to vagal stimulation was markedly attenuated during paired pacing and after acetylstrophanthidin; the percent reductions in pressure caused by vagal stimulation were 5.0 and 9.4%, respectively. The potentiation of the response to vagal stimulation during increased cardiac sympathetic activity probably represents a specific adrenergic-cholinergic interaction. • When ventricular myocardial contractility is enhanced by sympathetic neural activity, the negative inotropic effect of efferent vagal stimulation is potentiated (1). It has not yet been determined whether the greater

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Section: Levy Zieskesupporting

confidence: 45%

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

Levy

Zieske²

1969

Circulation Research

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“…Gremels (1935) produced evidence of this in the cat under chloralose, and similar observations have been made by Abdon, Hammarskjold & Nielsen (1938) and Perry & Reinert (1954). The sites of action might be two.…”

supporting

confidence: 55%

“…Not many attempts to study this question have been found in the literature. Effects of vagal stimulation on perfused isolated heart preparations have been described by a number of workers (Cullis & Tribe, 1913;Middleton, 1947;Perry and Talesnik, 1953;Perry & Reinert, 1954), but of these only Middleton made a statement concerning the length of time his preparations worked satisfactorily. He perfused the cat's heart and found that vagal effects were obtained for 6 hr provided the heart remained in situ, but when the heart was isolated, vagal effects were not obtained after 10-30 min.…”

mentioning

confidence: 99%

“…just sufficient to abolish the effect of vagal stimulation; this concentration did not appreciably diminish the effect of ACh in five out of ten experiments and did not abolish it in any. Perry & Reinert (1954) found that hexamethonium when perfused through the heart of the cat in a concentration of 3 x 10-4 g/ml., and when perfused through the heart of the guinea-pig in a concentration of 5 x 104g/ml. abolished the inhibitory effect of ACh.…”

mentioning

confidence: 99%

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The effect on the isolated rabbit heart of vagal stimulation and its modification by cocaine, hexamethonium and ouabain

McEwen¹

1956

The Journal of Physiology

390

150

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The experiments to be described have been concerned with the effect of vagus stimulation in the isolated heart and auricles of the rabbit. In the vagus-heart experiments the action of cocaine, of hexamethonium and of the cardiac glycoside ouabain was studied.As recently as 1953, Obrink & Essex state that 'it has become a widely accepted fact that stimulation of the vagi does not influence an isolated heart after 20-30 min. The reason for the transient response is not known.' Not many attempts to study this question have been found in the literature. Effects of vagal stimulation on perfused isolated heart preparations have been described by a number of workers (Cullis & Tribe, 1913;Middleton, 1947;Perry and Talesnik, 1953;Perry & Reinert, 1954), but of these only Middleton made a statement concerning the length of time his preparations worked satisfactorily. He perfused the cat's heart and found that vagal effects were obtained for 6 hr provided the heart remained in situ, but when the heart was isolated, vagal effects were not obtained after 10-30 min. Using the method now to be described it was possible to make observations for periods up to 9 hr. METHODS Rabbits were anaesthetized with urethane. The vagi were cut in the neck and dissected free from the surrounding tissue to the level of the aortic arch. The thoracic contents were excised and the cardiac ends of the vagi and the heart were cleared of as much tissue as possible, but leaving the root of the lungs and a short piece of trachea still adhering to the auricles. In this way the finer cardiac branches of the vagi were undisturbed. Finally, the aorta was cannulated, and the heart perfused by the usual Langendorff method. The preparation behaved satisfactorily provided that the final cleaning took no longer than 20 min.To prevent drugs from affecting the nerves, the perfusion fluid for the heart and the fluid bathing the stimulating electrodes were supplied by separate systems. These both included large chambers for saturating the solutions with the gas mixture. Having been warmed to a temperature of 350 C, fluid reached the heart with a pressure of 40 cm of water. The fluid supplied to the electrodes was heated by part of the water jacket which surrounded the heart. The flow of fluid

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“…Miscellaneous substances.-Cardiac glycosides increase the response of the SCG to submaximal preganglionic stimulation and to injections of ACh; larger doses depress ganglionic transmission (115,116,177). Stimulation of the ganglion by cardiac glycosides is not abolished by hexamethonium (115).…”

Section: Ganglion-stimulating Substancesmentioning

confidence: 98%

Pharmacology of Autonomic Ganglia

Trendelenburg¹

1961

Annu. Rev. Pharmacol.

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The Action of Cardiac Glycosides on Autonomic Ganglia

Cited by 16 publications

References 11 publications

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

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

The effect on the isolated rabbit heart of vagal stimulation and its modification by cocaine, hexamethonium and ouabain

Pharmacology of Autonomic Ganglia

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