Effect Of Strophanthin Research Articles

Correction of altered β-glucosidase activity induced by the toxic effect of strophanthin K and modeled cardiac decompensation with cordaron

Some biochemical mechanisms of the protective effect of cordaron with respect to strophanthin K cardiotoxicity in modeled cardiac failure are experimentally studied in random-bred male albino mice. Strophanthin K is shown to aggravate the disturbances in free and total activity of β-glucosidase and in lysosome membrane permeability in the heart that are characteristic of this pathology. In comparison with the toxic dose of cardiac glycoside, cordaron has an opposite effect on the functional state of the myocardial lysosome system.

Comparative evaluation of pharmacological effects of combined application of strophanthin with some antiadrenergic agents

Pharmacological effects of strophanthin combined with the action of some antiadrenergic agents were studied on isolated frog atria and on models of acute and subacute cardiac insufficiency in rats. The studies demonstrated appreciable differences in the effects of anapriline, cordarone and tropaphen on strophanthin toxicity and on its chronoinotropic properties.

Effect of strophanthin and digoxin on succinate and lactate dehydrogenase and membrane Na+, K+-ATPase activity in the heart of rats with experimental myocarditis

In experiments on 30 white mongrel adult rats of both sexes pathologic and reparative alterations in the kidney by the 30th day after recanalization of the ureter occluded for 1, 3, 7, 10, 15, 30 days have been studied using microdissection, light optic and electron microscopic methods. The fact has been established that in early times of HT (1 to 3 days) with the following reduction of urinary passage through the ureter (30 days), the canalicular-vascular formations of the kidney acquire normal morphological structure. In cases of more prolonged occlusion of the ureter (15 to 30 days) in the kidney noticeable destructive alterations prevail with replacement of parenchymatous elements by connective tissue.

Effect of strophanthin and digoxin on activity of an experimental epileptogenic focus in the frog hippocampus

It has been shown on frogs with epileptogenic focus induced by the injection of penicillin (1000 U in 0.4 ml) into the hippocamp that preinjection (or injection on the background of the functioning epileptogenic focus) of strophanthin (1.8 and 0.18 microgram/g) or digoxin (1.2 micrograms/g) into spinal lymphaticus sac led to a sharp increase in interparoxysmal epileptiform discharges and electrographic correlates of fits on the ECG. The influence of cardiac glycosides upon the epileptized cerebral neurons is thought to be associated with the capacity of these drugs to inhibit Na+, K+-ATPase of neurons and their axons resulting in the disturbance of cerebral mediator activity.

Combined inotropic effect of strophanthin and calcium on heart muscle

Combined inotropic effect of strophanthin and calcium on heart muscle

Effect of strophanthin and celanide on the cerebral circulation and metabolism

Effect of strophanthin and celanide on the cerebral circulation and metabolism

Effect of strophanthin and celanide on the course of development of postischemic cerebrovascular phenomena

In acute experiments on anesthetized cats with artificial respiration and isolated autohemoperfusion of the cerebral vessels by the pump of stabilized capacity (heparin was injected intravenously), cerebral ischemia was evoked by the stopping of the perfusion pump for 15 minutes. In the postischemic period (after perfusion resumption), 2 phases of the perfusion pressure (PP) changes were noted: at the beginning the PP lowering followed by the long-term increase (above the basic level). It is assumed that the PP changes reflect the time course of the development of suggestive postischemic cerebrovascular phenomena: hyper- and hypoperfusion. Preliminary intravenous injection (40-90 min before ischemia) of strophanthine and celanide (0.05 and 0.1 mg/kg) enhanced and extended the first phase and hampered the development of the second phase PP changes. Administration of strophanthine 90-120 min after ischemia (during the PP increase phase) did not alter the cerebrovascular resistance to the blood flow. Under these conditions the response of the cerebral vessels to strophanthine decreased as compared to that in intact (non-ischemized) cats.

Hemodynamic effects of strophanthin and pindolol in patients with hypertrophic cardiomyopathy.

The acute hemodynamic effect of 0.5 mg strophanthin and the subsequent effect of 1.O mg pindolol was studied in seven patients with symptomatic hypertrophic cardiomyopathy. Three women and four men, average age 39.1 years (range 15–61), underwent right and left heart catheterization with simultaneous pressure recordings in the left ventricle and the aorta. Strophanthin caused a slight increase in cardiac index, and increases in heart rate, in dp/dt and peak gradient. The Starling curve was shifted upward to the left in five of seven patients. Pindolol had essentially the opposite effects. Neither drug influenced systolic aortic flow. Pindolol led to a significant reduction in the mixed venous oxygen saturation and an increase in arteriovenous oxygen difference. We conclude that strophanthin had no deleterious effect in the present study and that it may be of benefit in the individual patient by increasing the atrial contribution to ventricular filling and by improving the contractility of the septum and the left ventricular wall in advanced stages of the disease. Further controlled studies are necessary to define the effect of drug treatment in hypertrophic cardiomyopathy.

Effect of some adrenergic agents on the cumulative effect of strophanthin

The effect of pharmacological blockade and stimulation of the adrenergic innervation on the toxicity and cumulative effect of strophanthin was studied in experiments on cats. Premedication with propranolol and preliminary reserpinization were found to increase tolerance to strophanthin and to weaken its cumulative effect. Isoprenaline sharply increased sensitivity to the cardiac glycoside, but in this case cumulation was totally absent.

Effect of strophanthin on metabolism of high-energy phosphorus compounds in the myocardium of rats in the early stages of individual development

Effect of strophanthin on metabolism of high-energy phosphorus compounds in the myocardium of rats in the early stages of individual development

Changes in mechanism of effect of strophanthin K on interferon production in cell cultures

Changes in mechanism of effect of strophanthin K on interferon production in cell cultures

Effect of strophanthin K on interferon production in a culture of chick embryonic fibroblasts

Effect of strophanthin K on interferon production in a culture of chick embryonic fibroblasts

Effect of spironolactone and norbolethone on the toxicity of digitalis compounds in the rat.

1. In the rat, both spironolactone (an antimineralocorticoid) and norbolethone (an anabolic steroid) inhibit the characteristic neuromuscular disturbances and the mortality produced by digitoxin, gitalin, proscillaridin, digoxin and digitalin. The corresponding effects of strophanthin K, ouabain and digitoxigenin could not be prevented.2. It may be concluded that, in our experimental conditions, both spironolactone and norbolethone counteract the toxicity of some, but not all, digitalis compounds tested and that both the protective steroids affect the toxicity of the same digitalis derivatives.3. This antidigitalis effect is not merely a secondary consequence of either antimineralocorticoid or anabolic potency because spironolactone lacks anabolic and norbolethone lacks antimineralocorticoid properties. Indeed, it appears that the ability to antagonize the toxicity of digitalis compounds represents a pharmacological property independent of all known steroid hormone actions, since spironolactone is virtually devoid of these.

Action of unithiol and cysteine on the renal effect of strophanthin

Action of unithiol and cysteine on the renal effect of strophanthin

Role of sulfhydryl groups in preventing and overcoming the toxic effect of strophanthin on the dog's heart

Role of sulfhydryl groups in preventing and overcoming the toxic effect of strophanthin on the dog's heart

Effect of strophanthin on the development of acute myocardial ischemia as shown by luminescence-histochemical methods

Effect of strophanthin on the development of acute myocardial ischemia as shown by luminescence-histochemical methods

The effect of strophanthin on the coronary circulation and cardiac oxygen intake in experimental myocarditis

Strophanthin given in therapeutic doses to healthy animals has no significant effect upon the coronary circulation and oxygen intake by the cardiac muscle. Toxic doses reduce the coronary circulation, the cardiac oxygen intake and the blood pressure; bradycardia appears. The dose of 20 μg/kg, which causes no changes in the coronary blood flow or the cardiac oxygen intake in the healthy animals, considerably reduces these values in animals with experimentally induced myocarditis. The different qualitative reactions occurring in response to strophanthin administration to animals with experimentally induced myocarditis may be partially explained by the increased cardiac sensitivity to strophanthin in this condition and the intensified excitation of the vagus nerves; the reflex character of the latter effect follows from experiments with vagotomy. The data on the increase in strophanthin toxicity and the different qualitative reaction of the coronary circulation observed in experimental myocarditis should be taken into consideration by clinicians treating diseases of the cardio vascular system with cardiac glycosides.

Effect of strophanthin G on oxidative metabolism in cardiac muscle.

PREVIOUS results published from this laboratory indicate that the increased mechanical efficiency (ratio of work output to energy input) apparent after the administration of non-toxic doses of cardiac glycosides to isolated spontaneously beating hearts is invariably associated with raised levels of oxidative metabolism1,2. Hajdu and Leonard3 recently directed attention to the possibility that such an increased rate of oxygen consumption could be due to the increased mechanical work output associated with the positive inotropic response rather than to the fundamental metabolic action of the glycosides themselves.

Effect of strophanthin on blood electrolytes and water-electrolyte excretion by kidneys in healthy subjects

An 23 herzgesunden weiblichen Versuchspersonen wurde in 2 Versuchsserien der Einflus von 0,35 mg K-Strophanthin (Kombetin Boehringer) auf die Wasser- und Elektrolytausscheidung der Niere und die Plasmaelektrolyte Natrium, Kalium und Chlorid untersucht. Es fanden sich folgende Ergebnisse.

Strophanthin-不整脈に關する研究

The therapeutic effect of drugs and the relationship between the effect of strophanthin and that of autonomic drugs were investigated on the rabbit's heart with arrhythmia induced by strophanthin using either the isolated, auricular strips with the pace-maker preserved or the organs in situ. It was recognized that this arrhythmia might be induced as the result. of drug poisoning in the cardiac muscle