Akademik Veri Yönetim Sistemi
Biotechnic & histochemistry : official publication of the Biological Stain Commission, cilt.98, sa.7, ss.479-491, 2023 (SCI-Expanded)
Citalopram is a selective serotonin re-uptake inhibitor (SSRI) antidepressant; it exhibits the greatest
cardiotoxic effect among SSRIs. Citalopram can cause drug-induced long QT syndrome (LQTS) and
ventricular arrhythmias. We investigated the protective effect of nicorandil, a selective mitochondrial
KATP (mito-KATP) channel opener, on LQTS and myocardial damage caused by citalopram in male rats.
In a preliminary study, we determined that the minimum citalopram dose that prolonged the QT
interval was 102 mg/kg injected intraperitoneally. For the main study, rats were divided randomly into
five experimental groups: untreated control, normal saline + citalopram, nicorandil + citalopram,
5-hydroxydecanoate (5-HD) + citalopram, 5-HD + nicorandil + citalopram. Biochemical and histologic
data from blood and heart tissue samples from six untreated control rats were evaluated.
Electrocardiographic parameters including QRS duration, QT interval, corrected QT interval (QTc)
and heart rate (HR) were assessed, and biochemical parameters including malondialdehyde,
reduced glutathione, glutathione peroxidase, superoxide dismutase were measured. We also
performed histomorphologic and immunohistochemical examination of heart tissue. Citalopram
prolonged QT-QTc intervals significantly and increased significantly the histomorphologic score and
proportion of apoptotic cells, but produced no differences in the oxidant and antioxidant parameters.
Nicorandil did not prevent citalopram induced QT-QTc interval prolongation and produced no
significant changes in oxidant and antioxidant parameters; however, it did reduce histologic
damage and apoptosis caused by citalopram.