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雌激素对促黄体生成素排卵前升高的促进作用观察

Observations on facilitation of the preovulatory rise of LH by estrogen.

作者信息

Kalra S P

出版信息

Endocrinology. 1975 Jan;96(1):23-8. doi: 10.1210/endo-96-1-23.

Abstract

Systemic levels of estradiol (E2) during the 4-day estrous cycle rise in a biphasic manner; slow elevations during diestrus II are followed by rapid increases during the early morning of proestrus (Kalra and Kalra, 1973). The relation of these alterations in systemic E2 levels to the proestrus surge of LH was investigated. Administration of progesterone (P 4 mg/rat) to rats at 2200 hr of diestrus II blocked ovulation and the surge of LH in the afternoon of proestrus. Injection of estradiol benzoate (EB, 5 mug/rat) 2 hr prior to, together with or following P treatment at 0300 hr of proestrus restored ovulation and the surge of LH. However, blockade of ovulation was not reversed if EB was administered at 0500 or 0800 hr of proestrus following P treatment on diestrus II. Similarly, bilateral ovariectomy at 2300 hr of diestrus II but not at 0300 hr or later on proestrus abolished the proestrus surge of LH. Apparently, the rapid rise in systemic E2 between 2300 hr of diestrus II and 0300 hrs of proestrus is crucial and serves to activate the neural "trigger" of preovulatory release of LH. The role of ovarian E2 secretion prior to 2300 hr of diestrus II in facilitation of neural "trigger" was studied. In the absence of endogenous E2 priming produced by ovariectomy at 0800 hr of diestrus II, EB injections at 2300 hr of the same day failed to restore the proestrus surge of LH. However, when ovariectomy was delayed to allow normal E2 priming through diestrus II, administration of EB shortly after ovariectomy at 2300 hr of diestrus II elicited the normal proestrus surge of LH. These results indicated that following the initial "priming" of central site(s) with low levels of circulating E2 during diestrus II, rapid elevations in ovarian estrogen secretion between 2300 hr of diestrus II and 0300 hr of proestrus facilitated the neural "trigger" of pituitary LH release during the critical period on proestrus.

摘要

在4天发情周期中,雌二醇(E2)的全身水平呈双相上升;在动情后期II期缓慢升高,随后在发情前期清晨迅速升高(卡尔拉和卡尔拉,1973年)。研究了全身E2水平的这些变化与促黄体生成素(LH)发情前期激增之间的关系。在动情后期II期22:00给大鼠注射孕酮(P 4毫克/只)可阻断排卵以及发情前期下午的LH激增。在发情前期03:00,在P处理前2小时、同时或之后注射苯甲酸雌二醇(EB,5微克/只)可恢复排卵和LH激增。然而,如果在动情后期II期P处理后,在发情前期05:00或08:00注射EB,则排卵阻断无法逆转。同样地,在动情后期II期23:00进行双侧卵巢切除术可消除发情前期的LH激增,但在发情前期03:00或更晚进行则不会。显然,在动情后期II期23:00至发情前期03:00之间全身E2的快速升高至关重要,它激活了LH排卵前释放的神经“触发因素”。研究了动情后期II期23:00之前卵巢E2分泌在促进神经“触发因素”方面的作用。在动情后期II期08:00进行卵巢切除术导致缺乏内源性E2启动的情况下,在同一天23:00注射EB未能恢复发情前期的LH激增。然而,当卵巢切除术推迟以允许通过动情后期II期进行正常的E2启动时,在动情后期II期23:00卵巢切除术后不久注射EB引发了正常的发情前期LH激增。这些结果表明,在动情后期II期循环E2水平较低对中枢部位进行初始“启动”之后,动情后期II期23:00至发情前期03:00之间卵巢雌激素分泌的快速升高促进了发情前期关键时期垂体LH释放的神经“触发因素”。

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