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Results for “Deslanoside”

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At least 19 recordsLinked to original sources
PubMed1978

Interaction of serotonin and deslanoside on cardiac rhythm in the cat.

The present study was performed to determine whether increases in the tissue content of serotonin creatinine SO4 in the periphery would influence the arrhythmogenic effect of deslanoside. This was accomplished by infusing serotonin into anesthetized cats exposed to a subarrhythmic dose of deslanoside, determining doses of deslanoside required to produce ventricular tachycardia and ventricular fibrillation, and determining ventricular pacemaker rate (obtained during vagal-induced sinus node suppression). It was found that animals receiving serotonin creatinine SO4 plus deslanoside exhibited a greater increase in ventricular rate during sinus node suppression than with 5-HT infusion alone. No corresponding increase in ventricular pacemaker rate during sinus node suppression was observed with creatinine SO4 plus deslanoside. In addition, the dose of deslanoside to produce ventricular fibrillation in these animals was significantly correlated with the increase in ventricular pacemaker rate seen during th 5-HT infusion in the presence of deslanoside. Studies were also performed to determine whether the arrhythmogenic interaction of serotonin with deslanoside was associated with alterations in either cardiac tissue, blood or plasma levels of serotonin and 5-hydroxyindoleacetic acid. The data revealed a significant correlation between serotonin content in the left ventricle and the dose of deslanoside required to produce ventricular fibrillation. These results suggest that exogenous serotonin interacts with deslanoside to enhance the arrhythmogenic action of deslanoside.

Animals↗
PubMed1975

Antagonism of deslanoside-induced cardiotoxicity by combined nicotinic and muscarinic blockade of autonomic ganglia.

The effect of ganglionic blockade on cardiotoxicity induced by deslanoside (25 mug/kg i.v. at 15-minute intervals) was evaluated in Dial-urethane anesthetized cats. Electrocardiogram, blood pressure and pre- and postganglionic cardiac sympathetic nerve recordings were monitored. When deslanoside was given to control animals, 150 +/- 8.2 and 179 +/- 11.9 mug/kg produced ventricular tachycardia and ventricular fibrillation, respectively. Pretreatment of cats with either hexamethonium or atropine alone did not influence the doses of deslanoside required to produce ventricular tachycardia or ventricular fibrillation. However, pretreatment with the combination of hexamethonium and atropine significantly increased the dose of deslanoside needed to produce ventricular tachycardia (181 +/- 12.3 mug/kg) and ventricular fibrillation (219 +/- 12.3 mug/kg). Furthermore, administration of atropine to hexamethonium-pretreated cats intoxicated with deslanoside decreased deslanoside-induced postganglionic nerve activity. These results indicate that blockade of both nicotinic and muscarinic ganglionic transmission is essential for a protective influence against cardiotoxicity induced by deslanoside.

Animals↗
PubMed1979

Effect of in vivo deslanoside on the uptake of serotonin into platelets.

The purpose of our study was to determine whether deslanoside administered in vivo results in inhibition of the active transport of [3H]-serotonin into blood platelets. Experiments were performed in cats and arterial blood samples were taken prior to initiating deslanoside infusion and at the point when it appeared from the ECG that ventricular fibrillation was imminent. Toxic arrhythmogenic doses of deslanoside were found to produce a significant reduction in the uptake of [3H]-serotonin into platelets. This increase in free serotonin in plasma caused by inhibition of uptake may play a role in the cardiotoxicity of deslanoside.

Animals↗
PubMed1990

Determination of cardiac glycosides in digitoxin tablets and deslanoside injections by micro-HPLC.

A micro high-performance liquid chromatographic (micro-HPLC) procedure for the assay of digitoxin tablets and deslanoside injections has been developed. Micro-HPLC is performed on an ODS micro column, with acetonitrile-methanol-water (10:20:17) for digitoxin tablets and acetonitrile-water (21:70) for deslanoside injections. The effluent is monitored by UV absorption at 220 nm. Quantitation of cardiac glycosides in tablets and injections is carried out by the internal standard method. The composite assay results for digitoxin tablets and deslanoside injections provide average values of 101.2 and 99.9% with standard deviations of 1.2 and 0.93%, respectively. This micro-HPLC method is sensitive, quantitative, and reproducible. It is suitable for use in examining the content uniformity of pharmaceutical preparations.

Chromatography, High Pressure Liquid↗
PubMed1979

Comparison of hemodynamic effects induced by pentaformilgitoxin and deslanoside in patients with heart failure.

The effect of pentaformilgitoxin and deslanoside on heart rate, blood pressure and cardiac output was compared in six patients with heart failure. Pentaformilgitoxin caused an increase of cardiac output from 3361 ml/min to 4183 ml/min (p less than 0.01). Deslanoside induced a non significant increase of cardiac output from 3617 to 3848 ml/min. Heart rate decreased significantly by both drugs: the reduction was greater after deslanoside (from 93.7 to 77.5 beats/min) than after pentaformilgitoxin (from 92 to 85 beats/min). Both drugs caused a comparable increase in stroke volume.

Aged↗
PubMed1978

Effect of arrhythmogenic doses of deslanoside on the uptake of monoamines in brain tissue and in cardiac tissue.

The purpose of our study was to determine whether a toxic arrhythmogenic dose of digitalis administered to an in vivo preparation would affect the neuronal uptake of norepinephrine, serotonin and dopamine in brain tissue and norepinephrine in cardiac tissue. This was investigated by intoxicating anesthetized cats with deslanoside, removing cardiac and brain tissue at the onset of ventricular fibrillation, and examining the ability of brain tissue to accumulate [3H]-NE, [3H]-T-HT and [3H]-DA and cardiac tissue to accumulate [3H]-NE. It was found that deslanoside inhibited uptake of [3H]-NE into the left ventricle and [3H]5-HT into the area postrema. These selective effects may reflect greater blood flow to these regions or different sensitivities of the transport mechanisms for these amines. This inhibition of uptake into both left ventricular tissue and area postrema may contribute to some of the cardiovascular and emetic effects seen with digitalis drugs.

Animals↗
PubMed1990

Determination of deslanoside in antemortem and postmortem specimens. Unusual case report.

One case of the erroneous administration of deslanoside and high level of drug in antemortem plasma and postmortem specimens has been reported owing to the unusual surrounding circumstances. Deslanoside in antemortem plasma was determined by FPIA and the analysis was done by HPLC in the postmortem tissue samples. The analytical results and methods used in the examinations are discussed in the following paper.

Child, Preschool↗
PubMed1977

[Dromotropic effects of drug combinations. Initial results bearing on a combination of deslanoside and ajmaline].

The electrophysiological effects of the cardiotropic drugs have been studied in man by the agency of endocavitary electrocardiography. The effects of drug combinations, which are often prescribed therapeutically, have been studied less often. The authors report the results of a preliminary study of the combination of deslanoside with ajmaline in 26 patients; its effects were compared with those using each drug separately. This combination seems to have true dromotropic effects; although deslanoside alone, in the doses used, does not modify conduction below the bundle of His, it can still act synergistically with ajmaline at this level. A detailed study of the pharmacological effects as a function of the original status of conduction shows that at the level above the bundle His, the dromotropic action is quantitively less on healthy conducting tissue than on abnormal tissue. The effects of ajmaline on the conduction times below the bundle seem to be similar whether or not there is any conduction defect under basal conditions. The difficulties in obtaining and interpreting such measurements in man are discussed in the hope of arriving at a general protocol for studying drug combinations.

Adult↗
PubMed1979

[Creatine phosphokinase release from perfused cardiac muscle under hypoxic conditions. Effect of propranolol, verapamil, reserpine and deslanoside].

Experiments were undertaken to determine if some drugs (propranolol, reserpine, verapamil and deslanoside) have an effect on CPK release from hypoxic heart muscle. Hypoxia was induced in isolated Langerdorff perfused rabbit hearts by gassing the perfusate with 95% N2 + 5% CO2. Hypoxic induced damage of the rabbit heart muscle has been quantited in terms of the relase of the intracellular enzymes creatinephosphokinase (CPK) into the extracellular space. Propranolol was either added at the start of the hypoxic perfusion or the rabbit were pretreated with it. Verpamil, dl-propranolol and reserpine provided protection evidenced by a reduction of hypoxic induced CPK release, while lanatoside C and d-propranolol failed to prevent the hypoxic muscle from releasing CPK.

Animals↗
PubMed1992

Effect of digitalis on norepinephrine kinetics in congestive heart failure.

OBJECTIVE: The aim of this study was to test the hypothesis that digitalis glycosides would reduce sympathetic activity as reflected by forearm venous norepinephrine kinetics in patients with congestive heart failure. BACKGROUND: Digitalis glycosides have been reported to decrease sympathetic nervous system activity with baroreceptor sensitization in experimental animals. Such effects could be of therapeutic importance in congestive heart failure. METHODS: Double-blind randomized assessment was made of the effects of low dose intravenous deslanoside (Cedilanid-D, 0.002 mg/kg body weight) and vehicle on heart rate, arterial pressure, forearm blood flow, plasma norepinephrine, norepinephrine clearance and norepinephrine spillover in nine patients with stable congestive heart failure, New York Heart Association functional class II or III. Open label assessment of the responses to 0.6 mg of deslanoside was made in an overlapping group of seven patients. All measurements were made 30 and 60 min after intravenous injection of drug or vehicle and after 15 min of 30 degrees head-down tilt as a test of the sympathetic response to baroreceptor loading. RESULTS: Heart rate, arterial pressure and forearm blood flow were unchanged by low dose deslanoside. Heart rate decreased slightly with the 0.6 mg dose with the patients in the supine position. Norepinephrine spillover and clearance decreased with time on each study day in the supine position, but no effect was attributable to digitalis. Plasma norepinephrine and norepinephrine clearance and spillover all remained unchanged during head-down tilt on each study day. CONCLUSIONS: Nonpressor doses of deslanoside do not suppress sympathetic activity as reflected by venous norepinephrine and norepinephrine spillover in patients with congestive heart failure. Further, deslanoside did not normalize the sympathetic response to mild baroreceptor loading produced by head-down tilt. These data do not support sympathoinhibition through baroreceptor sensitization as a likely effect of digitalis in congestive heart failure.

Deslanoside↗
PubMed1987

Effect of digitalis on the diaphragm in anesthetized dogs.

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Animals↗
PubMedDate not supplied

Deleterious effects of taurine in cats with digitalis-induced arrhythmias.

An established model of digitalis toxicity was used to investigate the antiarrhythmic properties of taurine. I.v. doses of taurine ranging from 0.01 to 4.0 mmole/kg were ineffective in converting a deslanoside-induced arrhythmia to sinus rhythm. Indeed, taurine was found to aggravate the arrhythmia and in three experiments precipitated ventricular fibrillation. In addition, pretreatment with 5 mmole/kg taurine i.v. had no significant effect on the doses of deslanoside to produce ventricular arrhythmia and fibrillation.

Animals↗