Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARDIAC GLYCOSIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources
PubMed1976

[Effect of cardiac glycosides on isoprenaline-induced heart changes].

The authors carried out studies on rats to examine the influence of preliminary treatment with strophanitine G on myocardial necrosis, induced by isoprenaline, evaluated by the changes in the number of leucocytes, erythrocyte sedimentation rate and the activity of SGPT in the peripheral blood, by the changes in the cardiac frequency and ECG as well as by the histologic and histochemical changes in the myocardium. It was established that strophanitine G potentiated the cardiotoxic action of isoprenaline, evaluated by hamatological, biochemical, electrocardiographic and histologic changes. The authors discuss the possible mechanisms of this interaction between digitalis glucoside and isoprenaline.

Alanine Transaminase↗
PubMedDate not supplied

[Comparative study of the effect of cycloartane and cardiac glycosides on various parameters of myocardial metabolism in animals].

Administration of cycloartane (askendoside D-10 mg/kg, cyclosiversioside F-25 mg/kg) and heart glycosides (strophanthin K-0.36 mg/kg, celanide-1 mg/kg) for 3-10 days is found to exert unidirectional effect on the indices of carbon, lipid and adenine nucleotide metabolism in animal myocardium under study. Glycogen and ATP content increases under parallel decrease of lactate and nonesterified fatty acid content. Differences in the effect of cycloorthane and heart glycosides and especially on the indices of myocardial carbon metabolism were registered under more prolonged administration. Administration of heart glycosides in contrast to cycloorthane ones promotes a decrease of glycogen level and redox potential and increase of lactate content.

Adenosine Triphosphate↗
PubMed1976

[Concentration of cardiac glycosides in the heart and brain (author's transl)].

In cats the concentration of cardio-active glycosides in the heart and brain were investigated with trititum-labelled substances. Steady-state conditions were achieved by repeated i.v. injections of ouabain, digoxin, beta-methyldigoxin, digitoxin, and oleandrin over 5 days. 5 h after the last application glycoside concentrations were measured in plasma, urine, heart, cerebrum and cerebellum. Furthermore the metabolic pattern in these compartments was determined. 1. The glycoside concentration in the heart per g wet weight ranges only from 0.93 (oleandrin) to 1.88% (ouabain) of the daily administered dose per kg. 2. The concentrations in the brain show much higher differences between the diverse glycosides: ouabain with a concentration of 0.02%/g wet weight in the cerebrum shows the lowest and oleandrin with 1.60% the highest value. 3. By calculating the mean relative weights for the hearts (3.9 g/kg) and the brains (11.1 g/kg) 3.7% of the daily administered ouabain activity were found in the whole heart and only 0.18% in the whole brain. In contrast to these data the content of heart and brain after giving the more lipophilic oleandrin was 3.6% and 17.7% (!), respectively. 4. Under steady-state conditions the glycosides ouabain, digoxin, beta-methyldigoxin and digitoxin in heart and brain are mainly unchanged whereas oleandrin is transformed at a higher rate to polar metabolites.

Animals↗
PubMed1981

Tissue binding sites involved in quinidine-cardiac glycoside interactions.

Quinidine has been shown to alter pharmacokinetics of digoxin by displacing the glycoside from mutual binding sites which are stereospecific with respect to quinidine. Characteristics of the binding site involved in quinidine-digoxin interaction were studied further in guinea pigs and rats. In the anesthetized rat quinidine significantly increased digoxin, but not digitoxin or ouabain, concentration in plasma during an i.v. infusion of a radiolabeled glycoside. In the anesthetized guinea pig, quinidine markedly increased plasma digoxin, but not digoxigenin or dihydrodigoxin, concentrations as estimated from a competitive binding assay using [3H]ouabain and a partially purified Na+, K+-adenosine triphosphatase preparation. Plasma sodium and potassium concentrations were not altered by quinidine either in control or digoxin-treated guinea pigs. In anesthetized guinea pigs, the quinidine concentrations in plasma was 6.4 +/- 1.1 muM after a 260-min fusion of quinidine at a rate of 26 mumol/kg/hr in control animals and 7.9 +/- 1.6 muM in those which were simultaneously infused with digoxin at a rate of 0.2 mumol/kg/hr. Antiarrhythmic agents, lidocaine, DL-propranolol or verapamil, did not cause a significant change in plasma digoxin concentration in the anesthetized guinea pigs. These results indicate that the binding site involved in quinidine-digoxin interaction has a strict structural requirement with respect ot the glycoside. Additionally, of the four antiarrhythmic drugs, quinidine appears to be the only agent which interacts with digoxin.

Animals↗
PubMed1978

[Clinical experience with the cardiac glycoside Gitoformat (author's transl)].

Gitoformat, a new derivate of Gitoxin, was tested with 50, mainly geriatic patients with a manifested cardiac insufficiency. The initial treatment as well as a changeover from the usual glycosid-treatment after a renewed decompensation was without any problems. With a rate of success of 95 per cent the efficiency of this new glycosid can be classified as excellent. Side effects or incompatibility were consequences of overdosage. It is remarkable that also patients with a reduced renal function did not need a reduction in dose. At 10 patients the recompensation with Gitoformat continued after discharge over an observation period of 6 months. The maintenance dose had not to be changed, incompatibility or overdosage reactions didn't appear.

Aged↗
PubMed1980

[Effective concentration and dosage for cardiac glycosides].

The pharmacokinetic fundaments of the glycoside therapy with strophanthin, digoxin and digitoxin are described and compared with the traditional clinically oriented parameters total body stores, decay ratio and so on. Newly introduced is the parameter medium remaining duration in the circulation. A critical analysis of the hitherto cited values of the total body stores and the decay ratio established from the clinical effect shows that on the basis of pharmacokinetic calculations the corresponding values for digoxin and digotoxin need a great correction. The fully active quantity for digoxin lies between 0.5 and 0.8 mg and the subsiding share is 50%. The values for digitoxin lie at 0.9 mg and 9%. Furthermore the causes of the interindividual variability of the maintenance dose are discussed. According to the already existing international experiences an essential improvement of the therapy is possible, when the pharmacokinetically established effective constants are taken into consideration. Examinations of the inter- and intraindividual differences in the kinetics of the glycosides and the development of digoxin preparations with a high (i.e. constant) bioavailability may contribute to a further decrease of the frequency of toxic side-effects in future.

Biological Availability↗
PubMed1975

Studies on cardioactive steroids. III. Characterization of different cardiac glycosides by their effects on contractility and rhythmicity at different extracellular potassium concentrations.

In the present paper, the naturally occurring glycosides digitoxin, gitoxin, 16-acetyl-gitoxin, digoxin, cymarol, ouabain, and proscillaridin, and the semi-synthetic 16-epi-gitoxin and 16-acetyl-16-epi-gitoxin are investigated as to their inotropic action and their effects on rhythmicity at isolated spontaneously beating atria of the guinea-pig heart in dependence on the variation of the potassium concentration of the nutritive fluid ([K+]0: 1.34, 2.68, and 5.36 mM resp.). The major results are as follows. 1. Effects of raising [K+]0 from 1.34 to 2.68 mM: The range of the inotropically effective concentrations as well as the size of the maximum inotropic action are more or less strongly improved with all glycosides. The glycoside concentrations required to get inotropic maximum had to be increased to a high degree with proscillaridin and digoxin. The mean arrhythmia percentage occurring at the inotropic maximum is either decreased (gitoxin, 16-epi-gitoxin, digoxin, proscillaridin), unchanged (digitoxin, 16-acetyl-16-epi-gitoxin) or even increased (16-acetyl-gitoxin, cymarol, ouabain). The inotropic value is improved to a high extent with gitoxin only. 2. Effect of raising [K+]0 from 2.68 to 5.36 mM: The range of the inotropically effective concentrations is extended (digitoxin and cymarol) or diminished (proscillaridin), but remains essentially unchanged with most glycosides. The size of the maximum inotropic effect is increased with digoxin, ouabain and 16-epi-gitoxin, but decreased significantly with digitoxin and proscillaridin. The glycoside concentrations required to produce the inotropic maximum are essentially unchanged with the exception of 16-epi-gitoxin, 16-acetyl-gitoxin and ouabain. The mean arrhythmia percentage at the maximum inotropic effect is dramatically reduced with digoxin, cymarol and proscillaridin. The inotropic value is improved with all glycosides except digitoxin. 3. Evaluation of the various glycosides: When judged on the basis of the range of inotropically effective concentrations, the maximum inotropic effect, the mean arrhythmia percentage at the inotropic maximum and the inotropic value, the best first three glycosides include 16-epi-gitoxin and digoxin. 16-Epi-gitoxin and its 16-acetate show that most favourable relationship between the effect on contractility and rhythmicity. The cause of the differential actions of the structurally-different glycosides on contractility and rhythmicity is hypothesized to be due to divergences in structure and/or conformation of the receptor areas of (Na+ + K+)-ATPase of contractile and excitable cells.

Animals↗