acetylstrophanthidin/heart failure

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Acetylstrophanthidin-induced reflex inhibition of canine renal sympathetic nerve activity mediated by cardiac receptors with vagal afferents.

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The present experiments were performed to determine whether digitalis-induced augmentation of cardiac receptor discharge could induce reflex reductions in renal sympathetic nerve activity. Intracoronary injection or epicardial application of acetylstrophanthidin (AS) in chloraloseanesthetized dogs

Reductions of myocardial Na-K-ATPase activity and ouabain binding sites in heart failure: prevention by nadolol.

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To study the changes in myocardial digitalis binding sites in heart failure, we measured myocardial ouabain binding sites, Na-K-adenosinetriphosphatase (ATPase) activity, and ventricular muscle mechanical responses to acetylstrophanthidin in dogs with right-heart failure (RHF) produced by tricuspid

The mechanics of left ventricular contraction in acute experimental cardiac failure.

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The effects of acute cardiac failure induced by pentobarbital or pronethalol on the basic mechanical properties of the intact left ventricle were examined in the dog, and the influence on auxotonic and isovolumic contractions of the increase in end-diastolic volume that usually accompanies cardiac

Peripheral arterial and venous responses to acetylstrophanthidin in patients with acute myocardial infarction.

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The peripheral arterial and venous responses to rapidly active acetylstrophanthidin (rather than the much slower digitalis) were studied in patients with acute myocardial infarction without congestive heart failure. In eight control patients placebo did not change mean blood pressure (BP), calf

Acetylcholine-induced reversal of canine and feline atrial myocardial depression during stretch, cardiac failure, and drug toxicity.

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Microelectrode and isometric recording techniques were used to evaluate the effects of acetycholine (ACh) on depressed isolated preparations of dog and cat atrial muscle. Atrial muscles were maintained at 36-37 degrees C with warmed Tyrode's solution and were stimulated at frequencies of 30 or

Ischemic heart failure: sustained inotropic response to small doses of I-epinephrine without toxicity.

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As a prelude to a study of severe ischemic heart failure, the therapeutic response of the ischemic ventricle to epinephrine and acetylstrophanthidin in nontoxic doses was determined in 24 intact anesthetized dogs undergoing a first episode of acute regional ischemia. A thrombotic obstruction was

Deficient production of cyclic AMP: pharmacologic evidence of an important cause of contractile dysfunction in patients with end-stage heart failure.

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We studied the effects of different classes of inotropic drugs on human working myocardium in vitro that was isolated from the hearts of patients with end-stage heart failure, and compared the responses to these drugs with those noted in muscles from nonfailing control hearts. Although peak

Decreased inotropic but relatively preserved relaxation response to cyclic adenosine monophosphate-dependent agents in myopathic human myocardium.

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BACKGROUND Increased intracellular concentrations of cyclic adenosine monophosphate (AMP) stimulate a positive inotropic and lusitropic response in healthy myocardial tissue. Heart failure results in an attenuated inotropic response to cyclic AMP-dependent agents. This study compares the inotropic

Dissociation of the inotropic effect of digitalis from its effect on atrioventricular conduction.

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The relation between sequential changes in left ventricular contractility and atrioventricular (A-V) nodal conduction and refractoriness was assessed in open chest dogs during intravenous administration of acetylstrophanthidin (5 mug/kg) at 5 minute intervals until toxic arrhythmias developed. At

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