小鼠病理性心肌肥厚伴随心外膜激活

Epicardium Is Activated in Cardiac Hypotrophy in Mice

目的研究心外膜细胞在小鼠病理性心肌肥厚中的性状变化。方法利用异丙肾上腺素(isoproterenol,Iso)诱导小鼠发生病理性心肌肥厚。腹腔连续注射7天和14天后,应用超声和麦胚凝集素(WGA)染色检验心肌肥厚造模效果。使用心外膜细胞特异标记转基因小鼠(Wt1Cre ERT2/+;Rosa26 RFP/+)检测病理性心肌肥厚与心外膜激活之间的联系。结果 (1)在注射Iso后,小鼠心重比有上升趋势,14d上升明显(P<0.05)。7d心功能出现代偿性增强(P<0.05),14d心功能衰弱。(2)心肌细胞的轮廓变大,转基因小鼠的免疫荧光发现病理性心肌肥厚中心外膜被激活。结论在Iso引起的病理性心肌肥厚中心外膜细胞被显著激活。表明心外膜可能在病理性心肌肥厚进程中发挥着重要作用。

Objective To study the characters of epicardium in mice cardiac hypotrophy（CH） induced by isoproterenol（Iso）. Methods The cardiac hypertrophy model was established in mice by injecting with Iso（30mg/kg/d, ip）. After 7 days and 14 days, these animals were assessed by echocardiography and wheat germ agglutinin（WGA） stain. Results of the transgenic mice（Wt1Cre ERT2/＋; Rosa26RFP/＋） whose epicardium is specifically marked suggested that the epicardium is activated in CH. Results（1） After injecting Iso, the heart weight ratio of mice was elevated, especially after the injection for 14 days（P〈0.05）. There was a significant compensatory increase of cardiac function in 7 days injection group（P〈0.05）, but after 14 days of injection, there came a decrease of cardiac function.（2） The area of cardiomyocytes became larger and the activation of epicardium was observed by the immunofluorescence of transgenic mice. Conclusion The significant activation of epicardium suggests that epicardium may play an important role in CH induced by Iso.