Chen Y M, Wright P J, Lee C S
Department of Veterinary Science, University of Melbourne, 250 Princes Highway, Werribee, Victoria 3030, Australia.
J Reprod Fertil Suppl. 2001;57:407-14.
The aims of this study were: (i) to establish a reliable model for the study of cystic endometrial hyperplasia in ovariectomized bitches; and (ii) to assess the roles of oestrogen and progesterone in the pathogenesis of irritant-induced cystic endometrial hyperplasia. Greyhound bitches (n = 15) were ovariectomized and divided into five groups (n = 3 per group). After 3-4 weeks, oestradiol benzoate (0.6-4.8 micrograms kg-1, i.m.) was administered twice a day for 12 days to the bitches in group 1, followed by progesterone (0.2-1.8 mg kg-1, i.m.) twice a day for 30-33 days. These dosages were chosen to mimic the plasma hormone concentrations of a normal oestrous cycle. A silk suture was inserted by laparotomy into the left uterine horn 12 days into the simulated dioestrus (determined by vaginal cytology) and necropsy was performed after a further 12 days. For groups 2-5, the silk suture was positioned at ovariectomy. After a further 3-4 weeks, these bitches were treated with progesterone (group 2: 1.8 mg kg-1 i.m. twice a day), oestradiol benzoate (group 3: 0.6-4.8 micrograms kg-1 i.m. twice a day), oestradiol benzoate and progesterone together (group 4: previous dosages) or vehicle (group 5). Necropsies were performed after 12-13 days of treatment. Cystic endometrial hyperplasia was induced in the suture-containing uterine horns of all bitches in groups 1 and 4, and in two bitches in group 2. Cystic endometrial hyperplasia did not develop in any control (no suture) uterine horns, or in either uterine horn of the bitches treated with either oestradiol only or vehicle. These results indicate that progesterone is necessary for the development of irritant-induced cystic endometrial hyperplasia and that oestradiol potentiates the effects of progesterone. The protocol used for bitches in group 1 would be a suitable model for further studies of the pathogenesis of cystic endometrial hyperplasia.
（i）建立一个可靠的模型用于研究去卵巢母犬的囊性子宫内膜增生；（ii）评估雌激素和孕激素在刺激性囊性子宫内膜增生发病机制中的作用。灵缇母犬（n = 15）接受去卵巢手术，并分为五组（每组n = 3）。3 - 4周后，第1组母犬每天两次肌肉注射苯甲酸雌二醇（0.6 - 4.8微克/千克），持续12天，随后每天两次肌肉注射孕激素（0.2 - 1.8毫克/千克），持续30 - 33天。选择这些剂量以模拟正常发情周期的血浆激素浓度。在模拟黄体期第12天（通过阴道细胞学确定）经剖腹术将丝线缝合线插入左子宫角，再过12天后进行尸检。对于第2 - 5组，丝线缝合线在去卵巢时放置。再过3 - 4周后，这些母犬分别接受孕激素治疗（第2组：每天两次肌肉注射1.8毫克/千克）、苯甲酸雌二醇治疗（第3组：每天两次肌肉注射0.6 - 4.8微克/千克）、苯甲酸雌二醇和孕激素联合治疗（第4组：先前的剂量）或赋形剂治疗（第5组）。治疗12 - 13天后进行尸检。第1组和第4组所有母犬以及第2组的两只母犬中，含有缝合线的子宫角诱导出了囊性子宫内膜增生。在任何对照（无缝合线）子宫角或仅接受雌二醇或赋形剂治疗的母犬的任一子宫角中均未发生囊性子宫内膜增生。这些结果表明，孕激素是刺激性囊性子宫内膜增生发生所必需的，并且雌激素增强了孕激素的作用。第1组母犬所采用的方案将是进一步研究囊性子宫内膜增生发病机制的合适模型。
