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Res., Semmelweis University Medical School, Ulloi ut 78/a, Budapest 1082, Hungary \n Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, Netherlands \n Department of Electrical Engineering, Eindhoven University of Technology, Eindhoven, Netherlands \n Department of Physiology, Cardiovasc. Res. Inst. Maastricht, Maastricht University, Maastricht, Netherlands \n Inotek Pharmaceuticals Corporation, 100 Cummings Center, Beverly, MA 01915, United States \n Cited By :51 \n Export Date: 4 December 2020 \n CODEN: BCPCA \n Correspondence Address: Ivanics, T.; Dept. Hum. Physiol. Clin. Exp. 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Oxidant-induced cell injury involves the activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) and pharmacological inhibition of PARP has recently been shown to improve myocardial contractility in doxorubicin-induced heart failure models. The current investigation, by utilizing an isolated perfused heart system capable of beat-to-beat intracellular calcium recording, addressed the following questions: (1) is intracellular calcium handling altered in hearts of rats after 6-week doxorubicin treatment, under baseline conditions, and in response to oxidative stress induced by hydrogen peroxide exposure in vitro; and (2) does pharmacological inhibition of PARP with the phenanthridinone-based PARP inhibitor PJ34 affect the changes in myocardial mechanical performance and calcium handling in doxorubicin-treated hearts under normal conditions and in response to oxidative stress. 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