摘要
目的：探讨米非司酮对妊娠中期胎儿肝脏超微结构的影响。方法：将中期引产孕妇随机分为两组：对照组（水囊组）10例，实验组（米非司酮＋水囊组）15例。实验组按孕龄分为实验Ⅰ组（n=10，16—22周）和实验Ⅱ组（n=5，23—28周）。实验组口服米非司酮100mg，连服3d，行水囊引产，对照组只行水囊引产。胎儿娩出后取肝脏组织进行样本制备，然后在电镜下观察肝脏组织细胞的超微结构。结果：肝脏组织细胞的超微结构有改变，且孕龄越小，超微结构改变越明显：①肝细胞肿胀，可见细胞连接；②大部分肝细胞核空化；③胞质空化，内可见少量粗面内质网及线粒体，脂褐素和糖原颗粒散在于细胞质内；④部分线粒体肿胀、空化、嵴断裂；⑤细胞之间有淋巴细胞浸润。结论：米非司酮可以引发胎儿肝脏组织的缺血缺氧性改变。
Objective To explore the effect of Mifepristone on the ultrastructure of the fetal liver in the second trimester pregnancy induced labor. Method 25 normal pregnant women were randomly divided into two groups： the control group （n = 10, average gestation of 22 weeks） was given waterbag induced labor alone and the test group （n = 15, average gestation of 22 weeks）was divided into two groups as the test group Ⅰ （n = 10, gestation of 16 -22 weeks）, the test group Ⅱ （n =5, gestation of 23 -28 weeks）. The test group took Mifepristone orally, 100mg per day for 3 days, then was given waterbag induced labor. After delivery of fetus, fetal liver was separated immediately for observation by transmission electron microscopic examination. Results Compared with the control group, the test group showed significant ultrastructure changes of the fetal liver and the earlier stage the fetus in, the more obvious ultrastructure changes were ： （1）liver cellswelled and cell junctions were found; （2）some nuclei cavitation was seen; （3）cell matrix cavitation, manipulus rough endoplasmic reticulum and mitochondria, scattered lipofusion and glycogen granules were showed; （4）mitochondria swelled and cristae disrupted; （5）leukomonocytes infiltrated. Conclusion Mifepristone can result in ischemia and hypoxia changes in the ultrastructure of the fetal liver in the second trimester pregnancy induced labor.
出处
《吉林医学》
CAS
2007年第3期314-315,317,共3页
Jilin Medical Journal
