Key result
Aconitine depresses early rhythmicity in cold-blooded auricles before triggering tachycardia and fibrillation-like responses.
Offers foundational model of aconitine-triggered tachyarrhythmia in isolated tissue; leaves open translation to mammalian or clinical arrhythmias.
The cold-blooded auricle under aconitine shows an early profound depression in rhythmicity but recovers in from 5 to 10 minutes to develop a high rate of spontaneous beating which may be considered a tachycardia for this preparation. Although arrhythmias do not appear spontaneously, a single, properly-timed stimulus to the auricle under aconitine initiates a multiple response which appears like ordinary fibrillation or flutter. The alterations in fundamental properties of the auricle which are required to elicit multiple responses favor a re-entrant rather than a focal mechanism of the induced arrhythmia.
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Tenney et al. (1954) studied Arrhythmia. Aconitine was evaluated on Rhythmicity and response to stimulus. Aconitine application to the cold-blooded auricle causes early rhythmicity depression followed by tachycardia, where a single stimulus initiates a multiple response resembling fibrillation or flutter.
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