Changes of the calcium tolerance in anthracycline treated mice.
Anthracyclines are effective antineoplastic agents inducing cardiomyopathy as a side effect. The mechanism of the anthracycline cardiotoxicity is not completely understood, but a disturbance of the Ca2+ -homeostasis seems to be involved. In our study we investigated the Ca2+ -tolerance in mice after a single administration of 2 mg/kg violamycin bI (vbI). Isolated hearts were perfused with increasing concentrations of Ca2+ until cardiac arrest. In the hearts of control animals the highest tolerable concentration was about 19 mM. 4 and 8 days after the vbI application 8 and 12 mM Ca2+, respectively, induced cardiac arrest. On the 12th day the Ca2+ tolerance was similar to control organs. 16 and 20 days after the vbI injection the highest tolerable Ca2+ -concentration sank again. On the 24th day the Ca2+ -tolerance was nearly the same as in controls.
Nachbar
A
A
Institute of Physiology II, Friedrich-Schiller University Jena, Germany.
Biewald
G A
GA
D000617:Aminoglycosides; D000818:Animals; D000900:Anti-Bacterial Agents / Q000009:adverse effects; D000903:Antibiotics, Antineoplastic / Q000009:adverse effects*; D002118:Calcium / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004361:Drug Tolerance; D005260:Female; D006323:Heart Arrest / Q000139:chemically induced; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D010477:Perfusion; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects; D017725:Ventricular Pressure / Q000187:drug effects
D000617:Aminoglycosides; D000900:Anti-Bacterial Agents; D000903:Antibiotics, Antineoplastic; C022171:violamycin BI; D002118:Calcium