Cardiac troponin T as a marker of myocardial damage caused by antineoplastic drugs in rabbits

被引:0
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作者
Michaela Adamcová
Vladimír Geršl
Radomír Hrdina
Milan Mělka
Yvona Mazurová
Jaroslava Vávrová
Vladimír Palička
Zdeněk Kokštein
机构
[1] Department of Physiology,
[2] Charles University Faculty of Medicine in Hradec Králové,undefined
[3] Šimkova 870,undefined
[4] 500 01 Hradec Králové,undefined
[5] Czech Republic e-mail: adamcova@lfhk.cuni.cz Tel.: +420-49-5816180 Fax: +420-49-33365,undefined
[6] Department of Pharmacology,undefined
[7] Charles University Faculty of Medicine in Hradec Králové,undefined
[8] Czech Republic,undefined
[9] Department of Pharmacology and Toxicology,undefined
[10] Charles University Faculty of Pharmacy in Hradec Králové,undefined
[11] Czech Republic,undefined
[12] Department of Biochemistry,undefined
[13] Charles University Faculty of Medicine in Hradec Králové,undefined
[14] Czech Republic,undefined
[15] Department of Histology,undefined
[16] Charles University Faculty of Medicine in Hradec Králové,undefined
[17] Czech Republic,undefined
[18] Institute of Clinical Biochemistry and Diagnosis,undefined
[19] Teaching Hospital,undefined
[20] Hradec Králové,undefined
[21] Czech Republic,undefined
[22] Department of Pediatrics,undefined
[23] Teaching Hospital,undefined
[24] Hradec Králové,undefined
[25] Czech Republic,undefined
关键词
Key words Cardiac troponin T; Daunorubicin; Oracin; Cardiomyopathy; Rabbits;
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摘要
Anthracycline derivatives are among the most effective antineoplastic drugs but their therapeutic use is limited by their adverse effects. The cardiac side-effects of antineoplastic drugs were investigated in rabbits in vivo from the viewpoint of release of cardiac troponin T (cTnT) measured by Elecsys Troponin T STAT immunoassay (Boehringer Mannheim, Germany). No increase in cTnT was found following administration of a single dose of daunorubicin (3 mg/kg i.v., n = 4). During development of daunorubicin-induced cardiomyopathy (daunorubicin 3 mg/kg i.v., once a week; maximum nine administrations, n = 7), the levels of cTnT were within the physiological range (i.e. cTnT < 0.1 μg/1) at the beginning of the experiment and before and after the 5th administration, but the pathological values of cTnT after the 8th administration in 43% animals (0.22 ± 0.08 μg/l) correlated with their premature death. In the control group, the levels of cTnT were always lower than 0.1 μg/l during the experiment. Following administration of a new antineoplastic drug – Oracin {6-[2-(2-hydroxyethyl) aminoethyl]-5,11-dioxo-5,6-dihydro-11H-indeno [1,2-c]-isoquinoline hydrochloride, 10 mg/kg i.v., once weekly, ten administrations, n = 7}, there was no increase in cTnT levels. These findings correlated with the PEP: LVET index, histological examination and no animal succumbing to premature death. It is possible to conclude that cTnT is a useful marker for the prediction of experimentally induced anthracycline cardiomyopathy and for the evaluation of cardiotoxic (and, possibly, cardioprotective) effects of new drugs in rabbits.
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页码:268 / 274
页数:6
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