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Protective effect of melatonin against myocardial injury induced by epinephrine

Vazan, Rastislav; Ravingerova, Tatiana.
J. physiol. biochem ; 71(1): 43-49, mar. 2015.
Artículo en Inglés | IBECS (España) | ID: ibc-133901
Epinephrine, in high doses, exhibits cardiotoxicity that is associated with excessive production of free radicals. Melatonin is antioxidant and free radical scavenger with cardioprotective properties. In our study, cardioprotective effects of melatonin against epinephrine cardiotoxicity were explored in the model of isolated rat heart. In the melatonin group, melatonin (50 μmol/l) was present in the perfusion solution during the whole experiment. In the control group, perfusion solution contained no melatonin. In both of the groups, after 30 min of initial perfusion, epinephrine was applied during 2 min directly into the heart and led to its strong stimulation. Changes in the heart function and arrhythmogenesis were evaluated before application of epinephrine and after the decline of its acute effects. No significant differences were observed during the initial perfusion. However, in the 15th and 20th minute after epinephrine application, indexes of ventricular contraction and relaxation were significantly higher in the melatonin group. Likewise, the values of the left ventricular developed pressure were significantly increased in this group in the 15th minute. These differences indicate better preservation of contraction and relaxation in the melatonin-treated group. Parameters of arrhythmogenesis—arrhythmia score, incidence and total duration of severe ventricular arrhythmias, were not significantly different between the experimental groups. However, their markedly lower average values in the melatonin-treated group suggest the reduction of electrical instability by melatonin. In conclusion, the obtained data confirm cardioprotective properties of melatonin and fill in the mosaic of information that can lead to the usage of melatonin as a therapeutic tool (AU)
Biblioteca responsable: ES1.1
Ubicación: BNCS