Key result
Ciprofloxacin decreased the force of contraction in isolated rat hearts (IC50 0.15 ± 0.04 μM) and significantly prolonged the QRS complex, QTc, and RR intervals while decreasing the VF threshold.
Why the study?
Does ciprofloxacin affect the contractile and electrical activity in isolated rat hearts?
Does ciprofloxacin affect the contractile and electrical activity in isolated rat hearts?
In isolated rat hearts, ciprofloxacin demonstrates negative inotropic effects and proarrhythmic electrical changes including QTc prolongation and decreased ventricular fibrillation threshold.
Suggests potential cardiotoxicity risk with ciprofloxacin; leaves open translation to human cardiac effects.
Context: Ciprofloxacin is the most commonly used fluoroquinolone and is prescribed as the antibiotic of choice in the treatment of several microbial infections. Some clinical reports have suggested that ciprofloxacin may induce QT-interval prolongation and Torsades de Pointes arrhythmias. This drug is a weak inhibitor of a rapid component of the cardiac delayed rectifier potassium current IKr, but there are few electrophysiological data available to assess whether ciprofloxacin has the potency to provoke QT prolongation and subsequent Torsades de Pointes arrhythmias. Aims: To evaluate the effect of ciprofloxacin on the contractile and electrical activity of isolated rat hearts. Methods: The Langendorff technique was performed in rat hearts, and the effects of ciprofloxacin (0.001 - 100 μM) were measured on the cardiac force of contraction and on the RR, QRS and QTc intervals. The arrhythmogenic potential and the ventricular fibrillation threshold were evaluated with ciprofloxacin. Results: Ciprofloxacin decreased the force of contraction of all hearts studied, in a concentration-dependent manner. The estimated IC50 for the inotropic negative effect was 0.15 ± 0.04 μM. Ciprofloxacin significantly prolonged the QRS complex, QTc and RR interval. Significant arrhythmic effects with ciprofloxacin were shown and the ventricular fibrillation threshold was decreased. Conclusions: These results suggest that ciprofloxacin exerted effects on cardiac Na+, K+ and Ca2+ channels. The actions of ciprofloxacin require further studies at the cellular level. These conclusions may account for clinical data that have been reported previously.
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Galán-Martínez et al. (2018) studied Cardiac actions of ciprofloxacin. Ciprofloxacin was evaluated on Cardiac force of contraction, RR, QRS and QTc intervals, arrhythmogenic potential, and ventricular fibrillation threshold. Ciprofloxacin decreased the force of contraction in isolated rat hearts (IC50 0.15 ± 0.04 μM) and significantly prolonged the QRS complex, QTc, and RR intervals while decreasing the VF threshold.
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