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PubMedDate not supplied

Digitalis glycosides accentuate the depressant effect of anoxia and reoxygenation on the cardiac myocyte: antagonism by amiloride.

The purpose of this study was to determine whether digitalis glycosides alter the effect of anoxia and reoxygenation on the cardiac myocytes and whether it could be modified by inhibition with amiloride. Cardiac myocytes aggregates were prepared from ventricles of 7 day old chick embryos and were maintained in culture. They were exposed to a 2 hr anoxia period followed by reoxygenation. Anoxia produced a significant reduction in contractile frequency. Ouabain, at low doses (10(-7) M and 10(-8) M), produced little effect in the absence of anoxia but produced a marked and significant (p less than 0.05) reduction in contractile frequency in the presence of anoxia. Myocytes exposed to anoxia stopped beating only in the presence of 10(-7) M and 10(-6) M ouabain and the time to cessation of spontaneous contraction was dependent on ouabain dose. Amiloride (10(-7) M or 10(-6) M) significantly (p less than 0.05) reduced but did not completely prevent the effect of ouabain. During reoxygenation, beating rate returned to base line in control cells and those exposed to ouabain (10(-8) M and 10(-7) M) but ouabain slowed the rate of recovery. This slowing of recovery, produced by ouabain, was prevented by amiloride. These findings indicate the potentially deleterious effects of digitalis glycosides in myocardial anoxia and reoxygenation and the ability of amiloride to oppose these adverse effects.

Amiloride↗

PubMed1977

A comparison of reversed-phase and partition high-performance liquid chromatography of some digitalis glycosides.

Comparison of the data for adsorption and reversed-phase chromatography of digitalis glycosides shows the complementary nature of the two modes of separation. The correct choice for a particular problem should make possible a rapid and good separation with simple isocratic systems. Detection limits vary between 10 and 100 ng per injection and permit the analysis of by-products even in low-dosage pharmaceutical formulations. Quantitation is easily possible with both chromatographic techniques using external standardization. The reproducibility for repetitive chromatograms is about 1% relative standard deviation for manual injections by loop injectors and is even significantly better for automatic injection. Reversed-phase chromatography can offer some advantages with regard to sample preparation of pharmaceutical formulations.

Cardenolides↗

PubMed1984

The basic mechanism of inotropic action of digitalis glycosides.

A broad survey of the experimental literature suggests that the only unifying concept of digitalis action is that these drugs, at pharmacologically relevant doses, bind with high affinity and specificity to sites on the NaK-ATPase complex that face the outer surface of nearly all eukaryotic cells. Alternative receptors, if they exist, have not been defined. As might be expected, a broad range of biologic effects results from this basic interaction. The clinical therapeutic effects of digitalis include enhancement of myocardial contractility and changes in the properties of the cardiac conduction system; the latter, in turn, result from both direct and autonomically mediated effects [44]. Autonomic effects involve alterations in both parasympathetic and sympathetic activity, and these are attributable to both central and peripheral neural mechanisms [44]. As we have reviewed, there is compelling evidence that one mechanism leading to sustained positive inotropic effects of digitalis glycosides in heart muscle is partial inhibition of sodium transport. Earlier evidence [16, 17] is now supported by electrophysiologic studies [29, 30, 45, 46], intracellular ion-sensitive microelectrode methods [47, 48], and ion flux measurements using radioisotope tracers [14, 15, 49]. Inhibition of myocardial monovalent cation transport has been documented in intact glycoside-sensitive animal models at doses and plasma and myocardial levels causing a positive inotropic effect without overt toxicity [12]. However, these findings do not preclude other mechanisms that may be operative in addition to, or in some circumstances instead of, myocardial Na-K pump inhibition. In the context of much seemingly conflicting evidence [35, 36, 37, 50, 51], the hypothesis advanced by Akera and Brody is of interest [17]. These authors suggest that interaction of subtoxic digitalis concentrations with myocardial NaK-ATPase reduces maximum sodium transport capacity, resulting in an enhanced transient increase in [Na]i during the early phase of the cardiac cycle. Such an increase in subsarcolemmal [Na+] could cause increased Ca++ influx via Na+-Ca++ exchange, with a consequent positive inotropic effect. If the Na+ increase were cyclic and not cumulative, cell Na+ content could return to normal by the end of a cycle due to enhanced turnover of unblocked Na-K pump sites. This hypothesis suggests a mechanism by which Na-K pump inhibition could cause a positive inotropic effect without any measurable increase in steady-state [Na+]i or decrease in [K+]i.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

Do digitalis glycosides still have a role in congestive heart failure?

It is apparent that the use of digitalis preparations, particularly digoxin, is important in patients with systolic left ventricular dysfunction, cardiomegaly, and congestive heart failure. Several historic studies suggest benefit, but more recently completed, well-designed, clinical trials have convincingly demonstrated that worsening congestive heart failure can be prevented and exercise capacity increased with digoxin. The precise dose and subsequent serum drug concentration giving the best safety-efficacy profile have not yet been determined. Importantly, the effect of digoxin on mortality is unknown. However, from a theoretic standpoint, this drug may fare well in ongoing mortality-end point clinical trials. The answer to the question, "Do digitalis glycosides still have a role in congestive heart failure?" is, therefore, absolutely!

Clinical Trials as Topic↗

PubMed1959