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    Effect of the selective mitochondrial KATP channel opener nicorandil on the QT prolongation and myocardial damage induced by amitriptyline in rats
    (Oxford Univ Press, 2023) Sahin, Orhan; Akturk, Gozde; Micili, Serap Cilaker; Doruk, Ozlem Gursoy; Karapinar, Fazilet; Hocaoglu, Nil; Ergur, Bekir Ugur
    Objectives The aim of this study is to evaluate the protective effect of nicorandil, a selective mitochondrial K-ATP channel opener, on QT prolongation and myocardial damage induced by amitriptyline. Methods The dose of amitriptyline (intraperitoneal, i.p.) that prolong the QT interval was found 75 mg/kg. Rats were randomized into five groups the control group, amitriptyline group, nicorandil (selective mitochondrial K-ATP channel opener, 3 mg/kg i.p.) + amitriptyline group, 5-hdyroxydecanoate (5-HD, selective mitochondrial K-ATP channel blocker, 10 mg/kg i.p.) + amitriptyline group and 5-HD + nicorandil + amitriptyline group. Cardiac parameters, biochemical and histomorphological/immunohistochemical examinations were evaluated. p < 0.05 was accepted as statistically significant. Key findings Amitriptyline caused statistically significant prolongation of QRS duration, QT interval and QTc interval (p < 0.05). It also caused changes in tissue oxidant (increase in malondialdehyde)/anti-oxidant (decrease in glutathione peroxidase) parameters (p < 0.05), myocardial damage and apoptosis (p < 0.01 and p < 0.001). While nicorandil administration prevented amitriptyline-induced QRS, QT, QTc prolongation (p < 0.05), myocardial damage and apoptosis (p < 0.05), it did not affect the changes in oxidative parameters (p > 0.05). Conclusions Our results suggest that nicorandil, a selective mitochondrial K-ATP channel opener, plays a protective role in amitriptyline-induced QT prolongation and myocardial damage. Mitochondrial K-ATP channel opening and anti-apoptotic effects may play a role in the cardioprotective effect of nicorandil.