Influence of Myocardial Catecholamines on the Cardiac Action of Ouabain

Swamy, V.C.; Hamlin, Robert L.; Wolf, Harold H.

doi:10.1002/jps.2600541022

Cited by 10 publications

(4 citation statements)

References 7 publications

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“…The mechanism by which the arrhythmogenic effect of cardiac glycosides is brought about is still obscure and the evidence for an adrenergic mediation of their cardiotoxic effects is quite conflicting. Thus SWAMY et al (1965) found that a continuous infusion of ouabain in the cat did not alter the atrial noradrenaline content significantly nor did pretreatment with reserpine have any effect on the arrhythmic or lethal dose of ouabain. On the contrary LOUBA- TIERES et al (1965) found that in the guinea pig a single dose of ouabain caused a marked depletion of myocardial noradrenaline.…”

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confidence: 87%

Evidence for Adrenergic Mediation of Ouabain induced Arrhythmias in the Guinea Pig

Hermansen¹

1969

Acta Pharmacologica et Toxicologica

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Oubain in a dose of7.5 pglmin. was infused intravenously into urethane anaesthetized guinea pigs weighing from 25&500 g. The incidence of cardiac fibrillation and the cardiotoxic dose (fibrillation, cardiac arrest) were determined in groups of (1) untreated controls, (2) adrenalectomized, (3) reserpinized, 5 mglkg subcutaneously, (4) reserpinized + adrenalectomized, (5) reserpinized -Inoradrenaline pretreated animals (100 pglkg intravenously 15 min. before ouabain). All animals were kept at a constant rectal temperature of 34". The pressor response to tyramine (0.1 and 1 mg/kg intravenously) was tested during the same experimental conditions. All animals died in fibrillation except those in (4) in which only 50 % showed fibrillation. The sensitivity to ouabain (minimal fibrillatory dose, LDlOO) was only slightly decreased in (2) while the LDlOO was increased from 239 k 10 ,ug/kg to 375 t 15 ,ug/kg in (3) and 466 f 17 pglkg in (4). Infusion of noradrenaline into reserpinized animals caused a partial recovery of the normal ouabain sensitivity as the LDlOO decreased from 375 k 15 pg/kg to 302 k 11 &kg (P < 0.001). The pressor response to tyramine showed features almost similar to the ouabain sensitivity except that the sensitivity to tyramine could not be regained by a noradrenaline infusion in reserpinized guinea pigs. The results indicate that the ouabain cardiotoxicity in the guinea pig is at least to some extent mediated through a release of catecholamines and may explain the species dependent difference in potency of some /I-adrenergic blocking agents on ouabain arrhythmias.

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confidence: 87%

Evidence for Adrenergic Mediation of Ouabain induced Arrhythmias in the Guinea Pig

Hermansen¹

1969

Acta Pharmacologica et Toxicologica

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“…This observation suggested to some investigators that catecholamines are necessary for the genesis of ventricular arrhythmia induced by digitalis materials (Roberts et al, 1963;Swamy et al, 1965). Although Roberts et al (Roberts et al, 1963;Roberts, Ehrreich & Levitt, 1965) have proposed that digitalis acts directly on the adrenergic nervous system, it is possible that physiological changes resulting from depletion of catecholamines-namely, fall in body temperature, heart rate or blood pressure-may account for the reserpine antagonism of the action of digitalis to induce ventricular arrhythmia.…”

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confidence: 99%

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confidence: 99%

“…A number of investigators have observed that reserpine, an agent which diminishes adrenergic nervous activity by catecholamine depletion, depressed ventricular arrhythmia induced by certain cardiac glycosides (Roberts, Ito, Reilly & Cairoli, 1963;Erlij & Mendez, 1964;Boyajy & Nash, 1965;Swamy, Hamlin & Wolf, 1965). This observation suggested to some investigators that catecholamines are necessary for the genesis of ventricular arrhythmia induced by digitalis materials (Roberts et al, 1963;Swamy et al, 1965). Although Roberts et al (Roberts et al, 1963;Roberts, Ehrreich & Levitt, 1965) have proposed that digitalis acts directly on the adrenergic nervous system, it is possible that physiological changes resulting from depletion of catecholamines-namely, fall in body temperature, heart rate or blood pressure-may account for the reserpine antagonism of the action of digitalis to induce ventricular arrhythmia.…”

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confidence: 99%

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