Effect of alterations in pulsatile luteinizing hormone release on ovarian follicular atresia and steroid secretion on diestrus 1 in the rat estrous cycle.
Effect of alterations in pulsatile luteinizing hormone release on ovarian follicular atresia and steroid secretion on diestrus 1 in the rat estrous cycle.
复制标题
脉动黄体生成激素释放的变化对大鼠动情周期中动情间期 1 的卵巢卵泡闭锁和类固醇分泌的影响。
DOI：
10.1095/biolreprod33.1.103
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发表时间：
1985
影响因子：
3.6
通讯作者：
Gallo,RV
中科院分区：
文献类型：
--
作者：
Devorshak-Harvey,E;Peluso,JJ;Bona-Gallo,A;Gallo,RV
本研究探讨了大鼠发情周期中初潮1期（D1; metestrus）搏动性黄体生成素（LH）释放对卵巢卵泡发育和雌二醇（E2）分泌的重要性。在D1上3小时采血周期开始前- 7.5小时单次注射促黄体生成素释放激素（LHRH）拮抗剂，通过降低LH脉冲幅度降低平均血液LH水平，而频率没有改变。在- 7.5和- 3.5 h连续注射完全消除脉动性LH分泌。两种治疗方法均不能改变直径大于150 μ的卵泡/卵巢总数、在150 ~ 551 μ之间的卵泡数量或血浆E2、黄体酮或促卵泡激素（FSH）水平。然而，两种LHRH拮抗剂治疗均显著增加卵巢闭锁卵泡的百分比。这些数据表明：1)脉动性LH释放是决定卵泡D1闭锁率的重要因素；2)单纯LH脉幅降低足以增加D1上卵泡闭锁的发生率；3)在D1上长达10小时的时间内缺乏脉动性LH释放不足以导致卵巢E2分泌下降，这很可能是因为闭锁过程处于早期阶段，尚未影响到足够数量的E2分泌颗粒细胞，从而降低卵泡分泌E2的能力；4)抑制或消除D1上脉动性LH释放与FSH分泌减少无关。
This study examined the importance of pulsatile luteinizing hormone (LH) release on diestrus 1 (D1; metestrus) in the rat estrous cycle to ovarian follicular development and estradiol (E2) secretion. Single injections of a luteinizing hormone-releasing hormone (LHRH) antagonist given at −7.5 h prior to the onset of a 3-h blood sampling period on D1 reduced mean blood LH levels by decreasing LH pulse amplitude, while frequency was not altered. Sequential injections at −7.5 and −3.5 h completely eliminated pulsatile LH secretion. Neither treatment altered the total number of follicles/ovary greater than 150 μ in diameter, the number of follicles in any size group between 150 and 551 μ, or plasma E2, progesterone, or follicle-stimulating hormone (FSH) levels. However, both treatments with LHRH antagonist significantly increased the percentage of atretic follicles in the ovary. These data indicate that: 1) pulsatile LH release is an important factor in determining the rate at which follicles undergo atresia on D1; 2) reductions in LH pulse amplitude alone are sufficient to increase the rate of follicular atresia on D1; 3) an absence of pulsatile LH release for a period of up to 10 h on D1 is not sufficient to produce a decline in ovarian E2secretion, most likely because the atretic process was in its early stages and had not yet affected a sufficient number of E2-secreting granulosa cells to reduce the follicle’s capacity to secrete E2; and 4) suppression or elimination of pulsatile LH release on D1 is not associated with diminished FSH secretion.