作者: Tibor Stracina , Iva Slaninova , Hana Polanska , Martina Axmanova , Veronika Olejnickova
DOI: 10.1620/TJEM.236.199
关键词:
摘要: Find fulltext at Masaryk University(opens in a new window)|View at Publisher| Export | Download More... Tohoku Journal of Experimental Medicine Volume 236, Issue 3, 19 June 2015, Pages 199-207 Long-term haloperidol treatment prolongs QT interval and increases expression of sigma 1 and IP3 receptors guinea pig hearts (Article) Stracina, T.a, Slaninova, I.b, Polanska, H.c, Axmanova, M.c, Olejnickova, V.a, Konecny, P.d, Masarik, M.c, Krizanova, O.e, Novakova, M.af Department Physiology, Masaryk University, Brno, Czech Republic b of Biology, c Department of Pathological Physiology, Czech Republic d Physiotherapy Rehabilitation, Masaryk e Center for Molecular Medicine, Slovak Academy Sciences, Bratislava, Slovakia f International Clinical Research Center, Animal St. Anne’s Faculty Hospital, View additional affiliations references (47) Abstract Haloperidol is a neuroleptic drug used medication various psychoses and deliria. Its administration frequently accompanied by cardiovascular side effects, expressed as interval prolongation occurrence even lethal arrhythmias. Despite these still prescribed Europe in clinical practice. binds to that are coupled with inositol 1,4,5-trisphosphate (IP3) receptors. Sigma are tissues, including heart muscle, they modulate potassium channels. Together with receptors, also involved in calcium handling tissues. Therefore, the present work aimed study effects long-term haloperidol administration on cardiac function. (2 mg/kg once day) or vehiculum was administered by intraperitoneal injection guinea pigs 21 consecutive days. We measured the responsiveness isolated from the haloperidol-treated animals additional application of haloperidol. Expression receptor IP3 receptors studied real time-PCR immunohistochemical analyses. caused significant decrease in relative heart rate prolongation interval of haloperidol-treated animals, compared control animals. The expression type 2 was increased both atria but not ventricles. The modulation receptors may lead altered calcium cardiomyocytes thus contribute changed sensitivity cells to arrhythmias.