Gao Lian-ru, Wang Zhi-guo, Zhang Ning-kun, He Sheng, Yao Lin, Ning Hao-yong, Kang Xiao-ling, Fei Yu-xing, Zhu Zhi-ming, Yang Ye
Department of Cardiology, Navy General Hospital, Beijing 100037, China.
Zhonghua Yi Xue Za Zhi. 2003 Oct 25;83(20):1818-22.
To investigate the feasibility and efficiency of fetal cardiomyocyte transplantation into the rat model of myocardial infarction.
Cardiomyocytes were isolated from aborted human embryos aged 12 - 16 weeks and cultured for 5 days to confirm their viability. Rat model of extensive myocardial infarction (MI) was established in 18 male Wistar rats by ligating the descending anterior branch of left coronary artery and the 18 rats were randomly divided into 2 groups: transplantation group (n = 7, 2 x 10(6) fetal cardiomyocytes were transplanted into the myocardial scar) and culture medium injection group (n = 6, culture medium was injected into the myocardial scar) 5 days after extensive MI was caused. Another 6 rats undergoing sham operation were used as controls. Echocardiography was performed before and 60 +/- 3 days after the implantation to assess the left ventricular (LV) remodeling and cardiac function. Then the rats were killed and their heart were harvested to undergo HE staining, immunohistochemical examination with antibody against human alpha-actin smooth muscle (SMA) isoform, and light microscopy.
Light microscopy revealed the presence of engrafted human fetal cardiomyocytes in the infarcted myocardium and the presence of nascent intercalated disks connecting the engrafted fetal cardiomyocytes and the host myocardium. The engrafted fetal cardiomyocytes were SMA positive. Serial echocardiography revealed that cell transplantation prevented scar thinning, LV further dilatation and dysfunction while the control animals developed scar thinning, significant LV dilatation accompanied by progressive deterioration in LV contractility.
Fetal cardiomyocytes can be implanted and survive in the infarcted myocardial cells, thus preventing the scar thinning, and LV further dilatation and dysfunction.
探讨将胎儿心肌细胞移植到大鼠心肌梗死模型中的可行性和效率。
从12 - 16周龄的流产人类胚胎中分离心肌细胞，并培养5天以确认其活力。通过结扎左冠状动脉前降支，在18只雄性Wistar大鼠中建立广泛心肌梗死（MI）模型，将这18只大鼠随机分为2组：移植组（n = 7，将2×10(6)个胎儿心肌细胞移植到心肌瘢痕中）和培养基注射组（n = 6，在广泛MI形成5天后将培养基注射到心肌瘢痕中）。另外6只接受假手术的大鼠作为对照。在植入前及植入后60±3天进行超声心动图检查，以评估左心室（LV）重构和心脏功能。然后处死大鼠，取出心脏进行HE染色、用抗人α-肌动蛋白平滑肌（SMA）亚型抗体进行免疫组化检查及光学显微镜检查。
光学显微镜检查显示梗死心肌中存在植入的人类胎儿心肌细胞，并且存在连接植入的胎儿心肌细胞与宿主心肌的新生闰盘。植入的胎儿心肌细胞SMA呈阳性。系列超声心动图显示，细胞移植可防止瘢痕变薄、左心室进一步扩张和功能障碍，而对照动物出现瘢痕变薄、左心室明显扩张并伴有左心室收缩力逐渐恶化。
胎儿心肌细胞能够植入梗死心肌细胞并存活，从而防止瘢痕变薄以及左心室进一步扩张和功能障碍。
