Key result
Tetracaine (25 to 50 micromol/L) abolished arrhythmogenic diastolic Ca2+ release and increased the amplitude of the systolic Ca2+ transient in rat ventricular myocytes exposed to isoproterenol.
Why the study?
Does tetracaine reduce arrhythmogenic diastolic Ca2+ release and increase systolic Ca2+ transient amplitude in rat ventricular myocytes exposed to isoproterenol?
Population
Rat ventricular myocytes
Comparison
Tetracaine (25 to 50 micromol/L) vs Isoproterenol (1 micromol/L) alone
Design
Preclinical
Authors
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Hypothesis-generating for RyR modulation in Ca2+-triggered arrhythmias; leaves open translation to human ventricular myocytes.
Does tetracaine reduce arrhythmogenic diastolic Ca2+ release and increase systolic Ca2+ transient amplitude in rat ventricular myocytes exposed to isoproterenol?
Reducing Ryanodine Receptor open probability with tetracaine abolishes arrhythmogenic spontaneous Ca2+ release and increases systolic Ca2+ transient amplitude in ventricular myocytes.
Venetucci et al. (2006) studied Arrhythmogenic Ca2+ release in calcium overload. Tetracaine vs. Isoproterenol alone was evaluated on Diastolic Ca2+ release and systolic Ca2+ transient amplitude. Tetracaine (25 to 50 micromol/L) abolished arrhythmogenic diastolic Ca2+ release and increased the amplitude of the systolic Ca2+ transient in rat ventricular myocytes exposed to isoproterenol.
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