Preliminary Research for Cellular Dysfunction in Adriamycin Cardiotoxicity

我们推测，在阿霉素心脏毒性中，心肌收缩力的细微异常可能先于心肌坏死，并反映为mRNA的变化。我们这项研究的目的是揭示在心肌坏死之前的心脏毒性早期可能发生的基因表达变化。本研究的主要目的是建立阿霉素毒性对心脏收缩功能障碍的体内模型。我们使用培养的成年心室大鼠心脏细胞，因为分离细胞的简单制备似乎是合适的，它将在这个复杂的问题上提供一个集中的方法来确定阿霉素心脏毒性的机制。成功收获成年大鼠肌细胞。在培养液中加入10^<-9> ~ 10^<-5> M的去甲肾上腺素，可使细胞收缩（或“收缩”）约20%。在培养液中加入1 ~ 103 ng/mL的阿霉素，24小时后无明显变化，但有大量细胞从培养皿中脱落。

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.