Lang G F, Etches R J, Walton J S
Biol Reprod. 1984 Mar;30(2):278-88. doi: 10.1095/biolreprod30.2.278.
Aminoglutethimide (AG), an inhibitor of steroidogenesis, was administered s.c. to 5 groups of laying hens at a dose of 200 mg AG/kg body weight 9 h before expected midsequence ovulation. This dose has previously been demonstrated to consistently block ovulation. The injection of AG was followed by s.c. injections of: Group 1, 1.0 mg progesterone; Group 2, 0.1 mg estradiol-17 beta; Group 3, 1.5 mg corticosterone, all at 6 h prior to expected ovulation; Group 4, 1.0 mg testosterone at both 8 h and 5 h before expected ovulation; and Group 5, 25 micrograms of ovine luteinizing hormone (LH) at 8 and 50 micrograms ovine LH at 6 h before expected ovulation. For each group, 4 control hens were injected with AG and the appropriate vehicle. Blood samples were taken at 1- or 2-h intervals from the time of AG injection to the expected time of ovulation. The hens were killed 4 h after expected ovulation and examined for the occurrence of ovulation. In all hens injected with vehicle, ovulation and the preovulatory surges of progesterone, testosterone, estradiol-17 beta and LH were inhibited. The plasma concentration of corticosterone was not reduced following an injection of AG. Four of 6 hens ovulated in response to injection of ovine LH, although neither endogenous LH nor progesterone were released. Thus, LH appears to play a direct role in follicular rupture and extrusion of the ovum. The administration of progesterone induced a significant and prolonged rise in LH, restoring AG-blocked ovulation in all hens treated (n = 6). Injections of testosterone restored LH release in all hens and ovulation in 2 of 7 hens treated. Three of 7 hens ovulated in response to the corticosterone injection. A preovulatory rise in LH was not observed, indicating that corticosterone may exert its ovulation-inducing effect directly on the mature follicle. Estradiol-17 beta did not restore LH release or ovulation in any of the hens treated with AG.
氨鲁米特（AG）是一种类固醇生成抑制剂，在预期排卵中期前9小时，以200毫克AG/千克体重的剂量皮下注射给5组产蛋母鸡。此前已证明该剂量能持续阻断排卵。注射AG后，皮下注射以下物质：第1组，1.0毫克孕酮；第2组，0.1毫克雌二醇-17β；第3组，1.5毫克皮质酮，均在预期排卵前6小时注射；第4组，在预期排卵前8小时和5小时各注射1.0毫克睾酮；第5组，在预期排卵前8小时注射25微克羊促黄体素（LH），在预期排卵前6小时注射50微克羊促黄体素。每组有4只对照母鸡注射AG和相应的赋形剂。从注射AG时到预期排卵时间，每隔1或2小时采集血样。在预期排卵后4小时宰杀母鸡，检查排卵情况。在所有注射赋形剂的母鸡中，排卵以及孕酮、睾酮、雌二醇-17β和LH的排卵前激增均受到抑制。注射AG后，皮质酮的血浆浓度未降低。6只母鸡中有4只对注射羊促黄体素产生反应而排卵，尽管内源性LH和孕酮均未释放。因此，LH似乎在卵泡破裂和卵子排出中起直接作用。注射孕酮导致LH显著且持续升高，使所有接受治疗的母鸡（n = 6）恢复了AG阻断的排卵。注射睾酮使所有母鸡恢复了LH释放，7只接受治疗的母鸡中有2只恢复了排卵。7只母鸡中有3只对皮质酮注射产生反应而排卵。未观察到LH的排卵前升高，表明皮质酮可能直接对成熟卵泡发挥其诱导排卵的作用。雌二醇-17β未能使任何接受AG治疗的母鸡恢复LH释放或排卵。
