Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without alteration of normal luteal function in rhesus monkeys
Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without alteration of normal luteal function in rhesus monkeys
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DOI：
10.1093/humrep/17.11.2825
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发表时间：
2002-11-01
影响因子：
6.1
通讯作者：
Stouffer, RL
中科院分区：
文献类型：
--
作者：
Duffy, DM;Stouffer, RL
背景：卵泡在排卵前产生的前列腺素（PG）似乎在局部起促进卵泡破裂和卵母细胞释放的作用。方法：为了确定是否PG合成抑制剂的管理直接进入灵长类动物卵泡将防止排卵事件，血清雌二醇被用来预测排卵日的LH激增恒河猴。在LH峰的前一天或当天，将溶媒（n = 9）、PG合成抑制剂吲哚美辛（10（-6）或10（-5）mol/l终浓度; n = 8）或10（-5）mol/l吲哚美辛+ 1 μ g/ml PGE（2）（n = 3）注射到排卵前卵泡的卵泡液中。在一些动物中，黄体期雌激素和孕激素在每日血清样品中测量。其他动物在卵泡注射后3天切除卵巢;检查卵巢以验证卵泡破裂和卵母细胞释放。研究结果：卵泡注射吲哚美辛[10（-6）mol/l（n = 4）或10（-5）（n = 4）mol/l终浓度]或溶剂（n = 6）未改变黄体功能。切除卵巢的连续切片检查证实了卵泡破裂，并且在溶媒注射的卵泡中不存在卵母细胞（n = 3）。在4/8个注射吲哚美辛的卵泡中观察到捕获的卵母细胞，尽管几个捕获卵母细胞的卵巢经历了卵泡破裂。在注射吲哚美辛+ PGE（2）的猴（n = 3）破裂的黄体化卵泡中未检测到卵母细胞。结论：卵泡给药吲哚美辛可以阻止卵母细胞释放，而不抑制卵泡破裂或破坏随后的黄体功能。PGE（2）预防吲哚美辛诱导的排卵障碍的能力表明，在灵长类动物中，局部产生的PGE（2）在卵母细胞释放过程中起着关键作用。
BACKGROUND: Prostaglandins (PG), produced by the follicle just before ovulation, appear to act locally to promote follicle rupture and oocyte release. METHODS: To determine whether administration of PG synthesis inhibitor directly into the primate follicle would prevent ovulatory events, serum estradiol was used to predict the day of the ovulatory LH surge in rhesus monkeys. On the day before or the day of the LH surge, vehicle (n = 9), the PG synthesis inhibitor indomethacin (10(-6) or 10(-5) mol/l final concentration; n = 8), or 10(-5) mol/l indomethacin + 1 mug/ml PGE(2) (n = 3) was injected into the follicular fluid of the pre-ovulatory follicle. In some animals, luteal phase estrogen and progesterone were measured in daily serum samples. Other animals were ovariectomized 3 days after follicle injection; ovaries were examined for verification of follicle rupture and oocyte release. RESULTS: Follicle injection of indomethacin [10(-6) mol/l (n = 4) or 10(-5) (n = 4) mol/l final concentration] or vehicle (n = 6) did not alter luteal function. Examination of serial sections of removed ovaries confirmed follicle rupture and the absence of oocytes in vehicle-injected follicles (n = 3). Trapped oocytes were observed in 4/8 indomethacin-injected follicles, though several ovaries with trapped oocytes had experienced follicle rupture. Oocytes were not detected in the ruptured, luteinizing follicles from indomethacin + PGE(2)-injected monkeys (n = 3). CONCLUSIONS: Follicular administration of indomethacin can prevent oocyte release without inhibition of follicle rupture or disruption of subsequent luteal function. The ability of PGE(2) to prevent indomethacin-induced ovulatory failure suggests a critical role for locally produced PGE(2) in the process of oocyte release in primates.