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Ce produit n'est pas destiné à diagnostiquer, traiter, guérir ou prévenir toute maladie. Ces déclarations n'ont pas été évaluées par la Food and Drug Administration.
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Ces informations sont fournies à titre éducatif uniquement et ne remplacent pas un avis médical professionnel, un diagnostic ou un traitement. Consultez toujours votre professionnel de santé avant d'utiliser des plantes, surtout si vous êtes enceinte, allaitez, prenez des médicaments ou avez une condition médicale.
Strophanthus gratus
West African liana whose seeds yield ouabain used by hunters as arrow poison and by cardiologists for heart conditions.
Strophanthus gratus is a West African liana whose seeds yield the cardiac glycoside ouabain, historically used as an arrow poison and in early cardiology for heart failure. Its modern use is limited to intravenous pharmaceutical ouabain for acute cardiac conditions, though it has largely been replaced by digoxin due to high toxicity. Key active compounds include ouabain, g-strophanthin, cymarin, and strophanthidin.
Ouabain selectively inhibits the Na+/K+-ATPase pump on cardiac myocyte membranes, increasing intracellular sodium. This reduces calcium efflux via the Na+/Ca2+ exchanger, leading to elevated intracellular calcium and enhanced myocardial contractility (positive inotropy). It also exhibits vagomimetic effects, slowing heart rate, and at toxic doses causes calcium overload, delayed afterdepolarizations, and severe arrhythmias.
West African liana whose seeds yield ouabain used by hunters as arrow poison and by cardiologists for heart conditions.
Strophanthus gratus is a West African liana whose seeds yield the cardiac glycoside ouabain, historically used as an arrow poison and in early cardiology for heart failure. Its modern use is limited to intravenous pharmaceutical ouabain for acute cardiac conditions, though it has largely been replaced by digoxin due to high toxicity. Key active compounds include ouabain, g-strophanthin, cymarin, and strophanthidin.
Ouabain selectively inhibits the Na+/K+-ATPase pump on cardiac myocyte membranes, increasing intracellular sodium. This reduces calcium efflux via the Na+/Ca2+ exchanger, leading to elevated intracellular calcium and enhanced myocardial contractility (positive inotropy). It also exhibits vagomimetic effects, slowing heart rate, and at toxic doses causes calcium overload, delayed afterdepolarizations, and severe arrhythmias.