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PubMed1987

Cardiac glycoside poisoning in sheep caused by Urginea physodes (Jacq.) Bak. and the isolated physodine A.

Urginea physodes (Jacq.) Bak., a species closely related to or possibly synonymous with U. pusilla, is described and its distribution given. Four bufadienolides were isolated from U. physodes and the approximated LD50 and cumulative effect of some of them determined in guinea pigs. The most toxic one proved to be mildly cumulative. Typical signs of acute cardiac glycoside poisoning, involving the locomotory, gastro-intestinal, respiratory and cardiac system, were seen in the field cases and/or were experimentally induced by the plant. Similar signs could also be induced by injecting the isolated bufadienolide, physodine A, to a sheep.

Animals↗
PubMed1988

Micro high-performance liquid chromatographic determination of cardiac glycosides in beta-methyldigoxin and digoxin tablets.

A micro high-performance liquid chromatographic (micro-HPLC) method has been developed for the assay of beta-methyldigoxin and digoxin tablets. Quantitation of cardiac glycosides in tablets was carried out by the incorporation of dexamethasone as an internal standard. The procedure consisted of disintegration of tablets, extraction with acetone-ethanol (9:1) and injection for micro-HPLC on an ODS micro column, using acetonitrile-water (28:72) for beta-methyldigoxin tablets and methanol-water (1:1) for digoxin tablets; the effluent was monitored by UV detection at 220 nm. The average values of the contents in beta-methyldigoxin and digoxin tablets were 99.6 and 100.2% of the labelled amounts, respectively. The proposed method is sufficiently precise and sensitive to examine the content uniformity of tablets.

Cardiac Glycosides↗
PubMedDate not supplied

Structure-activity relationships of an aminosugar cardiac glycoside, ASI-222 HCl, in the heart-lung preparation of the dog.

ASI-222 [3-beta-O-(4-amino-4,6-dideoxy-beta-D-galactopyranosyl) digitoxigenin HCl] is a semisynthetic aminosugar cardiac glycoside that has been shown to have a greater therapeutic index than ouabain or digoxin in dogs. We have compared the effects of ASI, digitoxigenin, digitoxigenin-beta-D-galactose, and digoxin in the dog heart-lung preparation. Minute work and stroke work were calculated. Controls were obtained before and after the hearts were failed with sodium pentobarbital. ASI-222 is about three times more potent than digitoxigenin and about twice as potent as digitoxigenin-beta-D-galactose in producing similar increases in the left ventricular stroke work. ASI-222 is about three times more potent than digoxin in creasing left ventricular stroke work. Our results indicate that the addition of an aminosugar group to the genin further increased potency over that observed with the addition of a single neutral sugar and prolonged the duration of activity in failing myocardial tissue.

Aminoglycosides↗
PubMed1997

High-performance liquid chromatography-ionspray mass spectrometry for the specific determination of digoxin and some related cardiac glycosides in human plasma.

An original method based upon high-performance liquid chromatography coupled to ionspray mass spectrometry (HPLC-ISP-MS) has been developed for the identification and quantification in plasma of several cardiac glycosides, namely digoxin, digitoxin, lanatoside C and acetyldigitoxin. After single-step liquid-liquid extraction by chloroform-2-propanol (95:5, v/v) at pH 9.5 using oleandrin as an internal standard, solutes are separated on a 4 microm NovaPak C18 (Waters) column (150x2.0 mm, I.D.), using a gradient of acetonitrile-2 mM NH4COOH, pH 3 buffer (flow-rate 200 microl/min, post-column split 1:3). Detection is done by a Perkin-Elmer Sciex API-100 mass analyzer equipped with an ISP interface. In most instances the major ion observed is not [M+H]+ as expected, but [M+NH4]+. The mean retention times (min) are: lanatoside C, 5.74; digoxin, 6.00; digitoxin, 8.08, oleandrin, 8.30, acetyldigitoxin, 8.66 and 9.01 (isomers alpha and beta, respectively). The lower limits of detection in single ion monitoring mode range from 0.15 ng/ml (alpha- and beta-acetyldigitoxin) to 0.60 ng/ml (lanatoside C), making the method less sensitive than radioimmunoassay, whereas it is much more specific.

Acetyldigitoxins↗
PubMed1987

Cardiac glycosides.

Despite continuous controversy associated with a variety of aspects of the pharmacology of the cardiac glycosides, it appears that these agents will continue to be widely used in the future. Current methods for the measurement of digoxin are unreliable and allow measurement of both cardioinactive metabolites of digoxin and endogenous digoxin-like substances. As a result, the therapeutic monitoring of digoxin concentrations should, for the most part, be limited to an assessment of patient compliance and confirmation of a clinical impression of drug toxicity.

Animals↗
PubMed1994

Suspected cardiac glycoside poisoning in elephants (Loxodonta africana).

Two young (< 2 years old) elephants (Loxodonta africana) died suddenly and simultaneously at Ongava Game Reserve bordering on the Etosha National Park, Namibia. Both elephants showed lung congestion, epi- and endocardial haemorrhages and hyperaemic areas in the mucosa of the stomach and small intestine. Histopathology of the myocardium showed multifocal degeneration and necrosis of muscle fibres accompanied by haemorrhages. Parts of the leaves of the alien plant Cryptostegia grandiflora (Asclepiadaceae) were found in the intestinal tracts of the elephants. These findings suggested that the elephants died from heart failure after ingesting this plant which contains cardiac glycosides.

Animals↗
PubMedDate not supplied

[Binding of cardiac glycosides by the erythrocytes of patients].

Digoxin and strophanthin K uptake by patients' red cells was investigated by the Rb-86 assay. It was found that digoxin and strophanthin K levels in red cells increased with augmentation of the drugs concentrations in plasma, the ratio of cardiac glycoside levels in red cells to their concentrations in plasma decreased. The degree of binding to red cells is more pronounced for strophanthin K than for digoxin.

Adult↗
PubMed1988

[Are cardiac glycosides advisable in the treatment of food poisoning].

Rheopolycardiological investigation of 76 patients with food toxinfections (FTI) showed that phasic changes of systolic indices in these diseases developed as a result of extracardiac hemodynamic disorders and were of adaptive nature. Strophanthin administration to 20 similar patients at the height of disease brought about no statistically significant changes in systolic indices. It was concluded that the use of cardiac glycosides was inappropriate for the treatment of FTI.

Adolescent↗
PubMed1986

Enhanced sympathetic activity as a mechanism for cardiac glycoside toxicity in hypomagnesemia.

Hypomagnesemia was induced in dogs by administration of furosemide (20 mg/kg/day) for 7 days. Following replacement of a concomitant loss of potassium, ouabain was infused at 1 microgram/kg/min until death. The inotropic response, sustained ventricular arrhythmias, and death all occurred at significantly lower ouabain doses in hypomagnesemic animals than in normomagnesemic dogs. Additionally, hypomagnesemic dogs exhibited an abrupt sympathetic discharge which could be interrupted by bilateral ablation of the stellate ganglia. These results suggest that the neuroexcitatory effects of cardiac glycosides are enhanced during hypomagnesemia.

Animals↗
PubMed1984

Spin-labeled ouabain as a probe for cardiac glycoside receptor/Na, K-ATPase.

We have synthesized a nitroxide spin-label derivative of the cardiac glycoside, ouabain. It has been tested on purified Na,K-ATPase from dog kidney as a probe to study the physico-chemical interactions of this class of drugs with receptor(s). Spin-labeled ouabain retained the biochemical properties of native ouabain as judged by dose response curves for inhibition of Na,K-ATPase activity and inhibition of [3H]-ouabain binding to receptor. Electron paramagnetic resonance spectra of the spin-labeled ouabain-Na,K-ATPase complex revealed the presence of two types of bound label with differing degrees of immobilization.

Animals↗
PubMed1982

The electrogenic sodium pump in guinea-pig ventricular muscle: inhibition of pump current by cardiac glycosides.

1. The inhibition of the electrogenic sodium pump in guinea-pig ventricular muscle by cardiac glycosides was studied with a voltage-clamp technique.2. Superfusion of the preparation with dihydro-ouabain (DHO) produced a reversible depolarization of up to 7 mV. When the membrane potential was clamped to a constant value near the resting potential application of DHO produced a corresponding current change in the inward direction which reached a steady state in less than 1 min.3. The drug-induced current change (I(D)) was found to be the result of a parallel shift of the current-voltage relation. The contributions of a change in extracellular K or intracellular Na to the measured I(D) were shown to be very small. From these findings and the results summarized below it was concluded that I(D) represents the blockage of the electrogenic pump current by DHO and that it is proportional to the number of drug molecules bound to the Na-K-ATPase in the intact cell.4. The dependence of I(D) on the concentration of DHO applied (5 x 10(-6)-8 x 10(-4) M) was found to be consistent with the predictions of the law of mass action for reversible one-to-one binding of the drug to the Na-K pump under equilibrium conditions. From a Scatchard-type plot the equilibrium dissociation constant (K(D)) of DHO was determined to be 4.6 (+/-2.3) x 10(-5) M.5. The steady-state pump current in the resting preparation was calculated to be 0.81+/-0.26 muA/cm(2). It contributed 6.4+/-0.9 mV to the resting potential in Tyrode solution containing 3 mM-K.6. In the smallest preparations used the measured time course of the onset and decay of I(D) agreed with the chemical kinetics of binding and unbinding calculated for various DHO concentrations. The rate constant of unbinding (k(2)) was found to be 3.4 (+/-0.7) x 10(-2) S(-1) and the average rate constant of binding (k(1)) was 7.4 x 10(2) M(-1) S(-1).7. By comparing the effects of ouabain and DHO in the same preparation the following estimates of the chemical constants of ouabain binding to the Na-K pump were obtained: K(D) approximately 1.5 x 10(-6) M; k(1) approximately 4 x 10(3) M(-1) S(-1); k(2) approximately 6 x 10(-3) S(-1).8. An analysis of the transmembrane movements of Na and K in the steady state showed that the measured pump current density is consistent with a counter-transport of 3 Na and 2 K ions.

Animals↗
PubMed1978

Effect of some Pteridine compounds on the Na+ + K+)-ATPase and on the cardiac glycoside receptor of human heart).

Pteridine compounds are known to block Na+-reabsorption and K+-secretion in epithelial cells (salivary duct of the rat), which actively transport Na+ and K+ against an electrochemical gradient. Furthermore, there have been reports on antagonistic effects of these substances in digitalis induced arrhythmias. Therefore the actions of triamterene (Jatropur, Dyrenium), the sulfuric acid ester and the methylether of p-hydroxytriamterene (OH-triamterene) and OH-triamterene on specific [3H] g-strophanthin (ouabain) binding and Na+ + K+)-ATPase activity of isolated human cardiac cell membranes were investigated. Triamterene, the sulfuric acid ester and the methylether of OH-triamterene inhibit (Na+ + K+)-ATPase activity only at very high concentrations (10(-5)--10(-4) M). OH-Triamterene does not inhibit this enzyme at concentrations lower than 10(-3) M. The specific binding of [3H] g-strophanthin to human cardiac cell membranes is inhibited half maximally at relatively high concentrations, too (10(-5)--10(-4) M). These results are rather indicative of unspecific effects due to membrane sites of action other than the (Na+ + K+)-ATPase or the cardiac glycoside receptor.

Adenosine Triphosphatases↗
PubMed1989

[Cardiac glycosides and calcium antagonists in the treatment of blood circulation insufficiency].

A study is presented of the main microcirculation values in comparison with systemic hemodynamics in patients with chronic circulatory insufficiency under the effect of complex therapy with dilanacin + corinfar and clift + corinfar. It was established that calcium antagonists reduce postloads and, thus, facilitate the cardiac work in overcoming general peripheral resistance of blood vessels supplementing the effect of cardiac glycosides in the direction of improvement of myocardial inotropism and increase of its propulsive force.

Calcium Channel Blockers↗
PubMed1990

Cross-resistance and biochemical characteristics of second-step mutants of HeLa cells resistant to cardiac glycosides.

From ouabain-resistant (OuaR) mutants of HeLa cells which do not show any cross resistance to the digoxin analog SC4453, stable second-step mutants resistant to either SC4453 or those exhibiting increased resistance to digoxin have been isolated. The mutants obtained exhibited highly specific cross resistance towards different cardiac glycosides (CGs) and, based on their cross-resistance patterns, contained more than one type of genetic lesion. Biochemical studies with these mutants showed that cellular uptake of 86Rb was inhibited by specific CGs to which they showed increased resistance. The mutants showed reduced binding of [3H]ouabain and [3H]digoxin in comparison with the parental OuaR cells and about 50-60% of the Na+, K(+)-ATPase activity in the mutant cell extract was highly resistant to inhibition by ouabain and digoxin. In contrast to the above changes, these mutants showed no evidence of amplification, enhanced transcription, or gross alterations in the genes for the alpha or beta subunits of Na+, K(+)-ATPase. These observations indicated that these mutants involved a second-specific alteration in Na+, K(+)-ATPase. In contrast to these mutants, Chinese hamster ovary cells, which naturally exhibit comparable levels of resistance to CGs, showed no significant binding of either [3H]ouabain or [3H]digoxin and all of their Na+, K(+)-ATPase activity was resistant to inhibition by CGs.

Animals↗