title: Therapeutic effects of ivabradine on hemodynamic parameters and cardiotoxicity induced by doxorubicin treatment in rat.
abstract: The aim of this study was to investigate the possible effects of ivabradine against doxorubicin (DOX)-induced cardiotoxicity in rats using hemodynamic parameters (electrocardiogram, heart rate (HR), and blood pressure), biochemical markers of oxidative stress, lactate dehydrogenase, aspartate transaminase, creatine kinase-MB, and histopathological analyses both in serum and tissue specimens. A total of 28 female rats were randomly assigned to 4 groups: (a) control (n = 6 rats), (b) DOX group (n = 7 rats), (c) DOX + ivabradine-treated group (n = 8 rats), and (d) ivabradine group (n = 7 rats). When the means of the four groups were compared, there was only a significant difference in the level of HR (p < 0.05). DOX treatment caused more HR elevation when compared to the control group, whereas ivabradine application after DOX treatment significantly reduced HR levels. Cardiomyocytes were revealed as normal histology in the light of both hematoxylin and eosin staining and immunostaining methods (caspase-3 and bcl-2) in all groups. The present study reported the therapeutic effects of ivabradine against DOX-induced cardiotoxicity accompanied by the hemodynamic and biochemical parameters.
authors.affiliation: Department of Cardiovascular Surgery, Inonu University, Malatya, Turkey. drmccolak@yahoo.com
authors.forename: M C
authors.initials: MC
authors.lastname: Colak
authors.forename: H
authors.initials: H
authors.lastname: Parlakpinar
authors.forename: S
authors.initials: S
authors.lastname: Tasdemir
authors.forename: E
authors.initials: E
authors.lastname: Samdanci
authors.forename: E
authors.initials: E
authors.lastname: Kose
authors.forename: A
authors.initials: A
authors.lastname: Polat
authors.forename: E
authors.initials: E
authors.lastname: Sarihan
authors.forename: A
authors.initials: A
authors.lastname: Acet
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D001219:Aspartate Aminotransferases / Q000097:blood; D001552:Benzazepines / Q000494:pharmacology / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002374:Catalase / Q000378:metabolism; D003402:Creatine Kinase / Q000097:blood; D004317:Doxorubicin / Q000633:toxicity*; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000502:physiology; D006331:Heart Diseases / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D000077550:Ivabradine; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000903:Antibiotics, Antineoplastic; D001552:Benzazepines; D002316:Cardiotonic Agents; D017392:Thiobarbituric Acid Reactive Substances; D000077550:Ivabradine; D004317:Doxorubicin; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase