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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.
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