Preliminary Research for Cellular Dysfunction in Adriamycin Cardiotoxicity

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We hypothesized that, in adriamycin cardiotoxicity, subtle abnormality of cardiocyte contractility might precede the cardiocyte necrosis and be reflected as the changes in mRNA.Our goal for this study is to disclose the changes in gene expression that might occur in the early stage of cardiotoxicity prior to cardiocyte necrosis. The primary purpose of the current research is to establish the in vivo model of cardiac contractile dysfunction on adriamycin toxicity. We utilized cultured adult ventricular rat cardiac cells, because the simple preparation of isolated cells seem to be appropriate and it would provide a focused approach in this complicated question to define the mechanism(s) of on adriamycin cardiotoxicity.Adult rat myocytes are successfully harvested. Adding noradrenaline of 10^<-9> to 10^<-5> M into the culture caused shrinkage (or "contraction") by about 20% Giving adriamycin of 1 to l03 ng/mL into the culture made no apparent change after 24 hours, but significant amount cells detached from the culture dish.