Disease relevance of strophanthidin

• To determine the efficacy of digitalis drugs in suppressing ventricular ectopic activity, 142 patients with frequent (greater than 1 per minute) ventricular premature beats underwent acetyl strophanthidin tolerance testing [1].
• Origin of acetyl strophanthidin-induced ventricular arrhythmias [2].
• To examine the origin of digitalis-induced ventricular tachycardia (VT), acetyl strophanthidin (AS) (25 mug/min) was perfused into a limited zone of myocardium in intact anesthetized dogs through a catheter placed fluoroscopically in the left anterior descending artery without ischemia [2].
• Contractures induced by treating resting muscles with 5 X 10(-5) M strophanthidin at 30 degrees C exhibited pronounced tension noise [3].
• The application of strophanthidin (10 microM) increased force and produced an intracellular acidosis [4].

High impact information on strophanthidin

• The inotropic action of epinephrine is accompanied by increased influx of calcium, while strophanthidin enhances the twitch without altering calcium influx during the action potential [5].
• Membrane potential, tension and aequorin luminescence were measured during exposure to elevated [Ca2+]0, strophanthidin and/or isoproterenol (to induce DADs), or cesium chloride (to induce EADs) [6].
• The inotropic effects of strophanthidin in Purkinje fibers and the sodium pump [7].
• Blockade of ATP-dependent Na(+)-K+ pump by both ouabain and strophanthidin enhanced hypoxia-induced membrane depolarization/inward current [8].
• With vesicles having relatively high intravesicular sodium concentration, (approximately 50 mM NaCl), the sodium pump effects an ATP-dependent sodium efflux coupled to sodium influx and to strophanthidin-sensitive ATP hydrolysis [9].

Chemical compound and disease context of strophanthidin

• 2. The retinal acidity appears to be due in part to the combined reactions of glycolysis and ATP hydrolysis, since anoxia greatly increased the pHo gradient, while superfusion with either glucose-free pyruvate solution or strophanthidin decreased this gradient [10].
• In electrically paced left atrial muscle, 0.3 mM theophylline reduced both the maximum developed tension observed in the presence of increasing concentrations of strophanthidin and the dose of this steroid that first elicited extrasystoles [11].
• The delayed afterdepolarizations or aftercontractions and contracture induced by epinephrine or strophanthidin were also inhibited by both anesthetics [12].
• Only phenytoin sodium displayed in vitro antiarrhythmic activity against strophanthidin-induced arrhythmias in guinea pig right atria [13].
• The antiarrhythmic effect of potassium and rubidium in strophanthidin toxicity [14].

Biological context of strophanthidin

• K-strophanthidin improved contractility indexes (peak of LV systolic pressure P < 0.001, max dP/dt + P < 0.05 and dP/dt P < 0.01) and worsened T constant and LV lowest diastolic pressure, (LVLDP) (P < 0.001 and P < 0.05 respectively) without changing early transmitral filling parameters [15].
• Moreover, a KCl solution containing amiloride (1 microM) and strophanthidin (100 microM) increased cell volume and suppressed the CBF increase, and then the subsequent removal of either amiloride or strophanthidin decreased cell volume and further increased CBF [16].
• 11. Embryos treated with strophanthidin during neurulation and then allowed to grow into tadpoles developed abnormal nervous systems [17].
• The elevation of end-diastolic pressure and reduced stroke volume in control dogs were not significantly altered by administration of strophanthidin [18].
• However, strophanthidin did antagonize the inhibitory action of cymarin which suggests that PTX and cardiac glycosides do not share an identical binding site but there may be some overlap [19].

Anatomical context of strophanthidin

• Na/K pump current was determined between -140 and +60 mV as steady-state, strophanthidin-sensitive, whole-cell current in guinea pig ventricular myocytes, voltage-clamped and internally dialyzed via wide-tipped pipettes [20].
• Strophanthidin-sensitive sodium fluxes in metabolically poisoned frog skeletal muscle [21].
• ATP stimulates Na transport into inside-out vesicles (IOVs) made from human red cell membranes; strophanthidin inhibits the ATP-stimulated transport [22].
• The effects of the inotropic drugs k-strophanthidin and dobutamine on left ventricular (LV) relaxation and early filling phase were compared in patients with coronary artery disease (CAD) and preserved systolic function [15].
• Inhibition of the Na pump with the cardiac glycoside strophanthidin prevents the normal fall in beta(3) during neurulation: beta(3) is maintained in the neural plate until the neural tube closes, but lost from the dorsal mesoderm [23].

Associations of strophanthidin with other chemical compounds

• Dissipation of the membrane potential with K+ and valinomycin resulted in stimulation of [14C]methylamine uptake, whereas both FCCP and valinomycin stimulated the strophanthidin-resistant ATPase activity [24].
• (b) The analysis of fluorescence experiments with the cardiotonic steroid strophanthidin indicates that the 5-iodoacetamidofluorescein label monitors the conformational transition (Na3)E1-P-->P-E2(Na2), which is accompanied by the release of one Na+ ion [25].
• The [Ca2+]-activated photoprotein aequorin was used to measure [Ca2+] in canine cardiac Purkinje fibers during the positive inotropic and toxic effects of ouabain, strophanthidin, and acetylstrophanthidin [26].
• Diltiazem had no effect upon tension development induced by acetyl strophanthidin in human myocardium or upon the Ca2+ sensitivity of chemically skinned atrial or ventricular fibers [27].
• 1 Sulphonate derivatives of k-strophanthidin and digitoxigenin were tested as active site-directed labels of Na+-K+-adenosine triphosphatase (Na+-ATPase) from guinea-pig heart [28].

Gene context of strophanthidin

• 3. In cell-attached patches addition of 100 microM strophanthidin to the bath increased both Gout and Gin [29].
• An increase of cell Na induced by strophanthidin during the Ca depletion phase has no effect on myoglobin release [30].

Analytical, diagnostic and therapeutic context of strophanthidin

• VF was induced either by perfusion with digitalis (strophanthidin, 30 microM) or by high-frequency electrical stimulation [31].
• [Ca2+]i increased from 69(SEM 5) nmol.litre-1 (n = 15) to 204(45) nmol.litre-1 (n = 14) after 10 min perfusion with 100 mumol.litre-1 strophanthidin [32].
• 1. The arrhythmogenic transient inward current, iTI, and contractions were recorded in isolated guinea-pig ventricular myocytes, after exposure to strophanthidin or low external K+ (0.5 mM), using a single-microelectrode voltage-clamp technique and an optical measure of contraction [33].
• The intracellular positions of the micropipette and microelectrode tips were verified by transient hyperpolarizations of the membrane potential with mucosal amiloride or by transient depolarizations with serosal barium or strophanthidin [34].
• Acetyl strophanthidin, 20 micrograms/kg, had a variable effect on duration of AF with beta-blockade but prolonged duration by 114 +/- 34%, p less than 0.05, with both vagotomy and beta-blockade.(ABSTRACT TRUNCATED AT 250 WORDS)[35]

References