Tehran University of Medical Sciences Acta Medica Iranica 0044-6025 49 4 2011 04 15 258 261 EN Mir-Jamal Hosseini Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Departments of Toxicology and Pharmacology, School of Pharmacy, Zanjan University of Medical Sciences, Zanjan, Iran. Azam Bakhtiarian Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. AND Faculties of Pharmacy, Pharmaceutical Sciences Research Center, Tehran University of Medical Sciences, Tehran, Iran. Peyvand Bina Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Sima Sabzeh-Khah Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Farzaneh Najar Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Abbas Pousti Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 2015 09 28 It has been reported that selective serotonin reuptake inhibitors (SSRIs) possess some cardiac effects. In the present study we have investigated the effect of paroxetine (PX), a potent SSRI agent, on spontaneously as well as ouabain-induced arrhythmia beating isolated guinea-pig atria. The Guinea-pig heart was rapidly removed; the auricles were dissected out in oxygenated modified Krebs solution. The rate and force of spontaneous contractions were recorded isometrically with a photosensitive transducer. PX (1-16 µg/ml) caused a dose-dependent decrease in the rate of contractions (14-70%) and contractile force (8-16%). Ouabain alone (1.2 µg/ml) produced arrhythmia at 7.2 ± 1.5 min and asystole at 20.1 ± 3.1 min. Pretreatment with PX (4 µg/ml) significantly increased the time of arrhythmia onset to 19.8 min. In addition, PX prolonged the duration of action beating from 20.1 ± 3.1 min to 43.1± 2.6 and delayed the occurrence of asystole. The pattern of contractile force by PX + ouabain treatment was more regular than that observed after administration of ouabain alone. The above findings may the probably be due to the inhibition of cardiac Na+ and Ca2+ channels or autonomic nervous system. Results also suggest that PX may reduce the membrane conductance through inhibition of ionic channels to prevent ouabain-induced arrhythmia. https://acta.tums.ac.ir/index.php/acta/article/view/3734 https://acta.tums.ac.ir/index.php/acta/article/download/3734/3709