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目的构建Wistar大鼠子宫直肠陷凹内膜异位症模型,对其病灶病理学形态及受孕率进行统计。方法采用异体移植方法在40只Wistar大鼠的子宫直肠凹陷处移植子宫组织,建立子宫直肠陷凹子宫内膜异位症动物模型,10只行假手术,8周后投放雄鼠,观察雌鼠的产仔率,于第15周取材剥取模型大鼠在位与异位子宫内膜组织,进行组织学观察。结果组织学上异位内膜的细胞形态呈增殖早期到分泌中期改变,和在位内膜呈增殖早期到分泌晚期改变发育不同步;模型组大鼠平均产仔数为6.02只,显著较假手术组8只及对照组为8.5只低(P<0.01)。结论 Wistar大鼠子宫内膜异位症内膜与在位内膜发育不同步,造成大鼠腹腔内环境异常,使受精卵着床变得更加困难,从而降低了大鼠的生殖能力。
Objective To construct the model of uterine rectocele and endometriosis in Wistar rats, and make statistics on its pathological morphology and pregnancy rate. Methods Uterine tissue was transplanted into the uterine rectum of 40 Wistar rats by allograft transplantation. Animal model of uterine rectum depression and endometriosis was established. 10 rats were sham operated. The rats were sacrificed 8 weeks later. Of the rate of birth, in the first 15 weeks of stripping model rats and ectopic endometrium, histological observation. Results Histologically, the morphology of ectopic endometrium was changed from early stage of proliferation to middle stage of secretion, and the eutopic endometrium showed an asynchronous change in development from early stage of proliferation to late stage of secretion. The average litter size in model group was 6.02, significantly higher than that of false Eight in the operation group and 8.5 in the control group were lower (P <0.01). Conclusion Wistar rat endometriosis intima and eutopic endometrium development is not synchronized, resulting in abnormal abdominal environment in rats, the fertilized egg implantation becomes more difficult, thus reducing the reproductive capacity of rats.