Fraser H M, McNeilly A S, Abbott M, Steiner R A
J Reprod Fertil. 1986 Jan;76(1):299-309. doi: 10.1530/jrf.0.0760299.
A dose of 100 microliter of a potent ovine LHRH gamma globulin inhibited ovulation in the cyclic rat when administered at 12:00 h on the day of pro-oestrus. A dose of 10 ml of the preparation was administered i.v. to female stumptailed macaques to achieve circulating antibody titres 3-4-fold higher than in the rat. In an ovariectomized macaque, this caused a marked fall in serum concentrations of LH to less than 10% of pretreatment values and also a significant, though less pronounced, fall in FSH. Six monkeys were treated with the LHRH gamma globulin during the mid-late follicular phase of the cycle. In 2 monkeys in which serum oestradiol concentrations were less than 100 pg/ml at the time of antibody administration, the rising oestradiol levels were abruptly suppressed and the normal mid-cycle LH surge failed to occur. Serum concentrations of LH and FSH declined to low levels for 8-10 days after which time normal follicular development occurred. In the remaining 4 monkeys in which follicular development was more advanced as indicated by serum oestradiol concentrations of greater than 100 pg/ml, the antibodies induced either a transient decline or had no effect on the rising serum concentration of oestradiol. An LH/FSH surge followed by a rise in serum progesterone occurred in these macaques. When the antibodies were administered to a further 6 macaques, which had also been treated with oestradiol benzoate during the early follicular phase to induce an LH surge, the neutralization of LHRH again failed to block the surge even when the dose of antibody was increased to 20 ml. The results show that LHRH antibodies were unable to block the LH surge in the macaque. They contrast with results obtained with LHRH immunoneutralization in the sheep, rat, hamster, mouse and bird and suggest that the ability of oestrogen to induce an LH surge by acting directly on the LHRH-primed anterior pituitary gland is more dominant in the primate.
在动情前期的12:00给处于发情周期的大鼠注射100微升强效绵羊促黄体生成素释放激素(LHRH)γ球蛋白,可抑制排卵。给雌性断尾猕猴静脉注射10毫升该制剂,以使循环抗体滴度比大鼠高出3 - 4倍。在一只卵巢切除的猕猴中,这导致血清促黄体生成素(LH)浓度显著下降至预处理值的10%以下,同时促卵泡生成素(FSH)也有显著下降,不过下降程度较轻。6只猕猴在周期的卵泡中晚期接受LHRHγ球蛋白治疗。在抗体注射时血清雌二醇浓度低于100皮克/毫升的2只猕猴中,上升的雌二醇水平被突然抑制,正常的周期中期LH峰未能出现。LH和FSH的血清浓度在8 - 10天内降至低水平,之后卵泡正常发育。在其余4只猕猴中,血清雌二醇浓度大于100皮克/毫升表明卵泡发育更成熟,抗体要么使上升的血清雌二醇浓度短暂下降,要么对其没有影响。这些猕猴随后出现LH/FSH峰,接着血清孕酮升高。当给另外6只在卵泡早期也用苯甲酸雌二醇治疗以诱导LH峰的猕猴注射抗体时,即使将抗体剂量增加到20毫升,LHRH的中和作用仍未能阻断该峰。结果表明,LHRH抗体无法阻断猕猴的LH峰。这与在绵羊、大鼠、仓鼠、小鼠和鸟类中通过LHRH免疫中和获得的结果形成对比,表明雌激素通过直接作用于LHRH预处理的垂体前叶来诱导LH峰的能力在灵长类动物中更为突出。