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PubMedDate not supplied

[Influence of kordaron, anaprilin, dimedrol and riboxin on the hemodynamic effects of strophanthin in experimental heart failure].

In experiments on 183 rats it was shown that cordarone, anapriline, dimedrol and riboxine increasing in experimental cardiac insufficiency tolerance to the cardiotoxic effect of strophanthin differ significantly by their influence on the hemodynamic effects of this cardiac glycoside. Cordarone increased intensity of the hemodynamic effects of strophanthin and accelerated their development. Under the action of anapriline and dimedrol the stimulating effect of strophanthin on hemodynamics decreased to a much lesser degree than its cardiotoxicity. Riboxine virtually abolished the hemodynamic effects of strophanthin.

Amiodarone↗
PubMed1985

[Characteristics of the action of strophanthin on central hemodynamics, pulmonary and intrahepatic blood circulation and myocardial contraction].

The effects of strophanthin treatment given in courses on the central hemodynamics, pulmonary, intrahepatic circulation and myocardial contractility were studied in 97 patients with decompensated chronic cor pulmonale depending on the hemodynamic type of circulation. In patients with CNPD and circulatory failure having the hypokinetic circulation, the treatment with strophanthin brought about improvement of the pulmonary and hepatic hemodynamics, increase in myocardial contractility, reduction of congestion. This may be accounted for by an elevation of the MOS, removal of the peripheral spasm on the part of the vascular system, elimination of prolonged venous congestion in the lungs and liver, and improvement of arterial blood flow in these organs. It was shown that in patients with hyperkinetic circulation, administration of strophanthin has an untoward effect on the hemodynamics in the lungs, liver and heart, thereby maintaining and increasing myocardial hyperfunction and venous hypervolemia. The data obtained indicate that it is inadvisable to prescribe strophanthin at early stages of the decompensated chronic cor pulmonale in patients with hyperkinetic circulation.

Adult↗
PubMed1984

[Correction of protein metabolism in myocardial infarction according to the results of radionuclide studies with 131-albumin during during treatment with a number of drugs (retabolyl, methyluracil, panangin, strophanthin) and combinations of them].

The effect of a series of drugs (retabolil, strophanthin, retabolil with strophanthin, retabolil with panangin , methyluracil with panangin ) on protein metabolism was investigated in 246 patients with acute myocardial infarction. Retabolil both alone and combined with panangin , and a methyluracil-- panangin combination were found to have anticatabolic and protein synthesizing effects. Strophanthin, when used in the acute period of myocardial infarction, contributes to an increase in the protein decay rate and a decrease in protein synthesis. When it is employed in combination with metabolism corrective agents (retabolil), the adverse effects of strophanthin mentioned above are eliminated.

Adult↗
PubMed1982

[Role of inflammation mediators in the etiology of hypersensitivity to strophanthin in various experimental heart diseases].

Effects of histamine and serotonin on strophanthine cardiotoxicity were examined in experiments on 312 cats. It was shown that inflammation mediators exert sympathomimetic action on the myocardium and potentiate strophanthine cardiotoxicity. These effects can be prevented by premedication with the beta-blocker alprenolol, antihistaminic, steroid and non-steroidal anti-inflammatory agents. It was disclosed that premedication with diphenhydramine, analgin and hydrocortisone might correct strophanthine tolerance decreased as a result of coronary artery occlusion. The conclusion is made that inflammation mediators play a role in the genesis of strophanthine hypersensitivity in experimental myocardial infarction.

Animals↗
PubMed1986

Single and combined myocardial pharmacodynamics of xamoterol, isoprenaline and g-strophanthin in the isolated rabbit heart.

The myocardial effects of g-strophanthin and the partial beta 1-adrenoceptor agonist xamoterol were compared to the effects of isoprenaline in the isolated spontaneously beating rabbit heart. Xamoterol and g-strophanthin both produced a distinct maximum increase in contractility as shown by the increase in isotonic contraction rate from 100 to 142% (pD2 7.51) and 151% (pD2 6.54), respectively, which was however less pronounced than the increase to 200% (pD2 7.81) caused by isoprenaline. The maximum chronotropic effect of xamoterol was moderate with a frequency increase from 100 to 128% (pD2 7.40) as was the increase in oxygen consumption to 130% (pD2 7.16), and no arrhythmias were seen. The positive inotropic range of g-strophanthin was very narrow (about 60-600 nM) and cardiac toxicity just overlapped and rapidly increased over this range. Xamoterol at a fixed concentration of 28 nM caused a rightwards shift of the isoprenaline concentration-response curves demonstrating the competitive beta 1-adrenoceptor blocking effect of the drug. G-strophanthin at a concentration of 268 nM acted additively with xamoterol with regard to maximum contractility and without causing any further increase in myocardial oxygen consumption except at the highest concentrations but there was a slightly increased nodal rhythm at xamoterol concentrations higher than about 20 nM.

Adrenergic beta-Agonists↗
PubMed1975

[Experimental heart muscle necorses in the rat after administration of 1-noreadrenaline and strophanthin. Light- and electron microscopic studies (author's transl)].

Female rats with a body weight of approximately 200 g regular show necroses of myocardial fibers after subcutaneous injection of 1-Noradrenaline (2.5 mg/kg body weight). After intraperitoneal premedication with Strophanthin k in a therapeutical dosage (2 X 10(-5 g/kg body weight), the increase in number and extent of the necroses is statistically significant. These findings argue against a preventive effect of Strophanthin k and can be explained by the mode of action of catecholamines and glycosides, as both substances, in a like manner, cause an increase in the mobilizable intracellular calcium of the myocardial fiber. Premedication with Strophanthin causes no alteration in the distribution pattern of necroses, nor in the electron-microscope findings in the case of myocardial necroses produced by Noradrenaline.

Animals↗
PubMed1976

[Influence of spirolactone on the myocardial potassium balance following strophanthin in man (author's transl)].

In order to examine the question, whether improved digitalis tolerance by Spirolactone may be partially a result of antagonism on myocardial potassium balance, 6 patients without clinical signs of heart failure were given 400 mg, 3 were given 200 or 300 mg Spirolactone orally daily and 6 patients received placebo during a 5 to 7 days period. During cardiac catheterization hemodynamics and serum potassium concentrations were determined repeatedly prior to and following intravenous administration of 0,375 to 0,625 mg Strophanthin. Injection of Strophanthin resulted in a significant drop in left ventricular enddiastolic pressure and a rise in dp/dt max. In the control group a significant increase in arterial and coronary sinus potassium concentration was observed. Myocardial potassium balance was definitely negative from the third to the eighth minute. Values in the group receiving Spirolactone did not differ significantly from the placebo group. It is suggested that therapeutic doses of Strophanthin resllt in a loss of potassium from the myocardium by inhibition of the Na+, K+ membrane ATPase not influenced by pretreatment with Spirolactone.

Arrhythmias, Cardiac↗
PubMed1973

Effects of potassium cyanide, strophanthin or sodium-free perfusion fluid on the electrical potential difference across the guinea-pig placenta perfused in situ.

1. The possible role of active transport of Na in generating the transplacental potential difference (p.d.) was studied in the guinea-pig placenta perfused in situ by testing the effects of strophanthin or KCN added to the perfusate or of Na-free perfusion fluid.2. The p.d. across the perfused placenta was about -20 mV, and was relatively steady during perfusion.3. Strophanthin (10(-5)M) slightly increased the p.d. In a concentration of 2 x 10(-6)M strophanthin was without significant effect.4. KCN (10(-3)M) decreased the p.d. When KCN was removed after a 30 min treatment the p.d. increased significantly exceeding the initial level. KCN (10(-4)M) slightly increased the p.d.5. Perfusion with Na-free fluid decreased the p.d. to a steady level of about 50-60% of the control values.6. Perfusion with Na-free fluid containing KCN (10(-3)M) for 30 min decreased the p.d. However, the effect did not seem different from the effect of KCN (10(-3)M) or Na-free fluid alone. When KCN was removed the p.d. significantly increased in spite of continued perfusion with Na-free fluid.7. Excepting the effect of KCN (10(-4)M), which could not be explained, the observations were found to be consistent with active transport of Na from foetal to maternal side of the placenta as a source of the p.d. The Na transport could account for about 40-50% of the p.d.

Animals↗
PubMed1975

[The effect of strophanthin following administration of homocardiac antigen to animals with experimental myocardial infarct].

A study was made of strophanthin sensitivity and hemodynamic effect of glycosidein immunization of rabbits with a homocardiac antigen on the 1st, 3rd and 5th days after the reproduction of myocardial infarction. The titre of anticardiac autoantibodies proved to decrease on the 10th day after the ligation of the coronary artery, and also there was a sharp reduction of strophanthin sensitivity by the values of the minimal lethal dose and the toxic one (causing cardiac arrhthmia). Changes in strophanthin tolerance under conditions of administration of the antigen from the myocardium with infarction are associated with the intensive immunopathological shifts in the heart.

Animals↗
PubMedDate not supplied

[The influence of inhibitors of kinin biosynthesis, prostaglandins and angiotensin II on the vascular and tubular effects of strophanthin in the rat kidney].

Strophanthin was shown to increase the blood flow in the external, internal zones of the cortex and the external medulla of the rat kidney without influencing the blood supply to the internal zone of the medulla. Contrikal eliminates the vasodilating effect of the drug in the mentioned zones of the renal tissue and significantly increases its natriuretic action. Indomethacin also prevents the hemodynamic shift occurring in the kidneys under the influence of strophanthin but fails to change the character of the natriuretic effect of the drug. Captopril exerts no influence on the increase of the blood flow in the external medulla but eliminates the vasodilating effect of strophanthin in the cortex and significantly potentiates its natriuretic action.

Angiotensin II↗
PubMed1991

[Effects of strophanthin K and beta-acetyldigoxin in vitro on energy transformation of myocardial contractile protein system in toxic-allergic lesions of the cardiac muscle].

Strophanthin K and beta-acetyldigoxin in vitro in concentration of 10(-6) M in TAM sharply increased the force generated by isolated myocardial contractile protein system (MCPS), and normalized the work performed by the system. This was accompanied by increase of ATP internal energy release (enthalpy) intensity, while a portion of energy, dissipating into heat did not increase proportionally. The mechanical efficiency of contractile process was normalized due to beta-acetyldigoxin, and exceeded the normal level due to strophanthin K effect. Strophanthin K proved a positive effect on quantitative and qualitative economy of MCPS energy utilization, while beta-acetyldigoxin effected, on the whole, extensively.

Acetyldigoxins↗
PubMed1990

Chronopharmacology of strophanthin and inderal: an experimental study.

Chronopharmacological investigations were performed in 54 guinea pigs and 126 white mice to explore their tolerance to arrhythmogenic and lethal doses of strophanthin, and changes in sensitivity to threshold antiarrhythmic dose of inderal during 24 hours. The investigations were carried out at a 4-hour interval, i.e., six times in 24 hours. The data obtained were processed using the approximation method to determine sinusoid fluctuations with an initially given period (cosinor analysis) and with an unknown period (non-linear least-square method in combination with the method of gradual approximation) on an EC 1045 computer and a DZ 28 microcomputer. It was found that strophanthin toxicity in guinea pigs and white mice reaches a maximum in the late evening, night and early morning hours. The acrophases of circadian rhythms of chronotolerance to the threshold arrhythmogenic dose of strophanthin, and those of chronosensibility to inderal are virtually identical.

Animals↗
PubMedDate not supplied

[Strophanthin sensitivity in disorders of cardiac blood supply, altered immunologic reactivity and under the influence of several pharmacologic agents].

Tests conducted with 125 cats demonstrated that occlusion of the coronary artery causes a higher sensitivity to the bathmotropic action of strophanthin, but does not have any effect on the magnitude of its lethal dose. The efficaciousness of potassium orotate and also of Na2EDTA in combinations with anapriline and isadrine, as regulators of the sensitivity to the toxic effect of strophanthin, was investigated. Immunization of cats with a homocardiac antigen was found to produce biphasic changes in the sensitivity to the toxic effect of strophanthin associated with the duration of antigenic stimulation.

Animals↗
PubMedDate not supplied

[Possibilities for the strophanthin pharmacological correction of cardio- and hemodynamic disorders in dogs in the early stage of experimental lung-heart failure].

Experiments on intact dogs and animals with an early stage of experimental cardiopulmonary insufficiency due to chronic pneumonia were made to study the action of strophanthine on the hemodynamics of the left and right ventricles and pressure in the pulmonary artery. Administration of the glycoside to animals with cardiopulmonary insufficiency increased the contractility of the right ventricle and the intensity of diastolic relaxation of both ventricles. Strophanthine was revealed to exert the prevailing effect on the cardiodynamics of the right ventricle both in intact dogs and in animals with experimentally induced pathology. Strophanthine increased pressure in the pulmonary artery, promoting the overload of the right ventricle to a less degree than convallotoxin.

Animals↗
PubMed1984

[Cardiotoxicity of strophanthin for rats and its correction with anaprilin in coronary-related and non-coronary-related damage to the myocardium and acute cardiac insufficiency].

It has been shown in rat experiments that non-coronarogenic injury to the myocardium induced by isadrin reduces the tolerance to the cardiotoxic action of strophanthine more powerfully than coronary artery occlusion. The physical overloading until complete exhaustion induced by swimming raises the cardiotoxicity of strophanthine to the same degree as non-coronarogenic injury to the myocardium. Hypersensitivity to strophanthine is successfully corrected by the beta-adrenoblocker anaprilin.

Animals↗
PubMedDate not supplied

[Inhibition of free-radical lipid peroxidation in myocardial infarct as affected by strophanthin].

It was shown in experiments on rats with experimental ischemic myocardial infarction that strophanthin inhibits free-radical lipid peroxidation, decreases (in mean and little doses) the ectopic activity of the myocardium, eliminates tachyarrhythmias arising in the presence of coronary occlusion, delays the appearance on the ECG of changes characteristic for acute myocardial infarction. In mean doses, strophanthin decreases the macrosize of the zone of infarction. It is recommended that strophanthin K (in mean and little doses) be included in a combined therapy of myocardial infarction.

Animals↗
PubMed1982

[Mechanisms of the development of strophanthin hypersensitivity in experimental myocardial infarct and its pharmacological correction].

The tolerance changes to strophanthin in cats were studied during 7 days after occlusion of the coronary artery along with the determination of the electrolyte concentration in different areas of the myocardium. It is shown that the acute disorder of the coronary circulation produces during 2 days considerable decrease of tolerance to the cardiotoxic action of strophanthin, which correlates with the electrolyte imbalance in the ischaemic and the adjacent areas of myocardium. Pharmacological analysis with the use of medicinal agents, possessing different properties established that the hypersensitivity to strophanthin in experimental myocardial infarction is an integral result of the influence of a number of factors, which when taken into account permit selection of rational medicinal correction of this phenomenon in different periods of acute myocardial ischaemia.

Animals↗
PubMed1981

[Factors that provoke strophanthin poisoning and its drug prevention].

The effect of various pathogenic factors and drugs on sensitivity to strophanthin and the possibility of pharmacoprophylaxis of toxicosis caused by this cardiotonic agent were studied in acute and chronic experiments on 375 cats. It is shown that impaired blood supply to the myocardium, toxic affection of the liver, sensitization with the cardiac antigen, and the effect of inflammation mediators, mineralocorticoids, and some antianginous agents reduce strophanthin tolerance. The altered sensitivity to strophanthin is successfully corrected with the beta-adrenoblocker alpheprol, hydrocortisone, analgin, dimedrol, and the anesthetic trimecaine.

Animals↗