A comparison of Josamycin with macrolides and related antibiotics on isolated rat atria

Tamargo, Juan; Miguel, B. De; Tejerina, M.T.

doi:10.1016/0014-2999(82)90073-5

Cited by 25 publications

(13 citation statements)

References 13 publications

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“…Resting tension was adjusted to 1.0 g and a 30 min equilibration period was allowed before control measurements were made. The techniques used and definitions of the sinus node recovery time and slow contractions are as previously described (Tamargo, De Miguel & Tejerina, 1982).…”

Section: Methodsmentioning

confidence: 99%

Electrophysiological effects of imipramine in non‐treated and in imipramine‐pretreated rat atrial fibres

Manzanares

Tamargo

1983

British J Pharmacology

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The effect of imipramine (Imip) in concentrations between 10−7M and 5 × 10−5M has been studied on rat atrial transmembrane potentials. In another group of experiments the effect of Imip was studied in atrial fibres from rats pretreated for 24 days with twice daily intraperitoneal injections of Imip 7.5 mg/kg or saline. In non‐treated atria Imip depressed action potential amplitude and Vmax, reduced the resting membrane potential and shifted the membrane responsiveness and recovery time curves downward and to the right. Imip also prolonged the action potential duration and the effective refractory period, lengthening the effective refractory period relative to action potential duration. Pretreatment with Imip decreased the resting membrane potential, amplitude and Vmax of the action potential and prolonged the effective refractory period. Further addition of Imip produced similar but more marked changes than in non‐treated animals. Imip suppressed the spontaneous atrial automaticity as well as the abnormal automaticity induced by BaCl2, aconitine, ouabain or isoprenaline. The drug produced a negative inotropic effect and depressed the amplitude of the slow contractions elicited by isoprenaline in K‐depolarized atria. It is concluded that even when the effects of Imip are similar to those of quinidine (group I of antiarrythmics), it also produces a reduction in Ca and K conductances.

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Section: Methodsmentioning

confidence: 99%

Electrophysiological effects of imipramine in non‐treated and in imipramine‐pretreated rat atrial fibres

Manzanares

Tamargo

1983

British J Pharmacology

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“…Likewise, an agonist effect on L-type calcium channels could have produced the combined HR and PR changes seen in this study. Moxifloxacin is not known to affect either I f or I Ca,L , though josamycin and erythromycin have been shown to inhibit transmembrane calcium flux [6]. …”

Section: Discussionmentioning

confidence: 99%

“…However, there is modest evidence in animal models that macrolide antibiotics [1,2,3,4,5,6] and, to a lesser extent, fluoroquinolone antibiotics [7] may increase HR, though there is only sparse clinical evidence for an HR effect in humans for these antibiotic classes [8,9]. The fluoroquinolone moxifloxacin is of particular interest because it is often used to treat infections associated with an already-increased HR, such as community-acquired pneumonia [10], and it is used as an active control in thorough QT (TQT) studies [11,12] QT is the electrocardiographic QT interval and reflects the duration of myocardial repolarization.…”

Section: Introductionmentioning

confidence: 99%

Moxifloxacin Increases Heart Rate in Humans

Mason

Moon

2017

Antibiotics

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(1) Background: We assessed the effect of moxifloxacin on heart rate, and reviewed the heart rate effects of other antibiotics; (2) Methods: A total of 335 normal volunteers had 12-lead electrocardiograms recorded at multiple time points before and during treatment with moxifloxacin and with placebo in seven consecutive, thorough QT studies of crossover design; (3) Results: The average baseline heart rate across the seven studies was 61.5 bpm. The heart rate after moxifloxacin dosing was analyzed at five time points shared by all seven studies (hours 1, 2, 3, 12 and 24). The maximum mean heart rate (HR) increase for the seven studies combined was 2.4 bpm (95% CI 1.6, 3.3) at hour 2. The range of mean maximum increases among the seven studies was 2.1 to 4.3 bpm. For the seven studies combined, the increase was statistically significant at all but the 24 h time point. The maximum observed individual increase in HR was 36 bpm and the mean maximum increase was 30 ± 4.1 bpm by time point and 8 ± 6.9 bpm by subject. Many antibiotics increase HR, some several-fold more than moxifloxacin. However, clinicians and clinical investigators give little attention to this potential adverse effect in the medical literature; (4) Conclusions: The observed moxifloxacin-induced increase in HR is large enough to be clinically relevant, and it is a potentially important confounder in thorough QT studies using moxifloxacin as an active control. More attention to heart rate effects of antibiotics is warranted.

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“…However, studies with dogs and cattle have revealed significant cardiovascular effects when tilmicosin is administered at doses Ͼ10 mg/kg, or by other routes (IM, IV, IP) [6,7]. Hypotension is probably a direct result of negative inotropic effects on the heart via interference with calcium cycling at the level of the sarcoplasmic reticulum, inhibiting calcium flux across membranes [8], and depletion of intracellular calcium. Many other macrolide antibiotics have been shown to have effects on myocardial calcium channels.…”

Section: Clinical Effectsmentioning

confidence: 99%

American Association of Poison Control Centers database characterization of human tilmicosin exposures, 2001–2005

Oakes

Seifert

2008

J. Med. Toxicol.

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A comparison of Josamycin with macrolides and related antibiotics on isolated rat atria

Cited by 25 publications

References 13 publications

Electrophysiological effects of imipramine in non‐treated and in imipramine‐pretreated rat atrial fibres

Electrophysiological effects of imipramine in non‐treated and in imipramine‐pretreated rat atrial fibres

Moxifloxacin Increases Heart Rate in Humans

American Association of Poison Control Centers database characterization of human tilmicosin exposures, 2001–2005

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