Abstract
Cardiac toxicity is a deadly condition caused by impaired cardiac activity similar to congestive heart failure (CHF). Doxorubicin (DOX) is a potent anticancer drug having a potential of myocardial damage [ [1] Minotti G. Menna P. Salvatorelli E. Cairo G. Gianni L. Anthracyclines: molecular advances and pharmacologic developments in antitumor activity and cardiotoxicity. Pharmacol Rev. 2004; 56: 185-229 Crossref PubMed Scopus (2860) Google Scholar ]. Doxorubicin induced experimental toxicity has been characterized by heart failure and anaemia [ [2] Noiri E. Nagano N. Negishi K. et al. Efficacy of darbepoetin in doxorubicin-induced cardiorenal injury in rats. Nephron Exp Nephrol. 2006; 104: e6-e14 Crossref PubMed Scopus (20) Google Scholar ]. In human patients, risks for the use of anthracyclines have been reported associated with cardiac death which is the most prevalent of QT prolongation that triggered Torsades de Pointes [ [3] Arbel Y. Swartzon M. Justo D. QT prolongation and Torsades de Pointes in patients previously treated with anthracyclines. Anticancer Drugs. 2007; 18: 493-498 Crossref PubMed Scopus (31) Google Scholar ]. The anaemia of CHF patient is evidently due to the excessive cytokine production [ [4] Silverberg D. Wexler D. Blum M. Wollman Y. Iaina A. The cardio-renal anaemia syndrome: does it exist?. Nephrol Dial Transplant. 2003; 18: viii7-12 PubMed Google Scholar ]. Pre-treatment with erythropoietin hormone alone protected the myocardium against DOX induced impaired cardiac function and cardiomyocyte apoptosis [ [5] Kim K.H. Oudit G.Y. Backx P.H. Erythropoietin protects against doxorubicin-induced cardiomyopathy via a phosphatidylinositol 3-kinase-dependent pathway. J Pharmacol Exp Ther. 2008; 324: 160-169 Crossref PubMed Scopus (93) Google Scholar ]. Therefore, the present study was designed to investigate the effects of ramipril and darbepoetin alfa, used either alone or together, on electromechanic activity of heart in an experimental toxicity model.
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