Benoit A M, Inskeep E K, Dailey R A
West Virginia University, Morgantown.
Domest Anim Endocrinol. 1992 Oct;9(4):313-27. doi: 10.1016/0739-7240(92)90019-t.
Three experiments were performed to study effects of decreased concentrations of estradiol-17 beta (E2) on lifespan and function of ensuing ovine corpora lutea (CL). In experiment 1, 52 follicles were collected from 10 ewes and placed into individual culture with 0 or .01 microCi 3H-androstenedione (10 ng; 3H-A) and 0, 10(-11), 10(-9), 10(-7), or 10(-5) M of a nonsteroidal aromatase inhibitor, CGS16949A (CGS). Concentrations of E2 secreted into the medium, and synthesis of estrogens as estimated by formation of 3H-water from 3H-A were decreased by 10(-5) and 10(-7) (P < .01), but not 10(-9) or 10(-11) M CGS. In experiment 2, luteolysis was induced in 24 ewes by injection of PGF2 alpha on days 5 to 10 of the estrous cycle (0 hr). Ewes received 0, 0.5, 1.0, 2.0 or 4.0 mg CGS per kg BW i.v. at -12, 0, 12 and 24 hr, and an ovulatory dose of hCG at 36 hr. Jugular (P < .001) and vena caval (P < .001) concentrations of E2 were decreased by CGS at all doses tested for 8 to 10 hr, but had returned to levels similar to control ewes by the time of the next injection. Concentrations of E2 around the time of the LH surge were similar in control and treated ewes. During the subsequent luteal phase, concentrations of progesterone (P4) were similar in control and treated ewes. Thus, transient decreases in E2 during the follicular phase were not deleterious to the subsequent luteal phase. In experiment 3, luteolysis was induced in 18 ewes by injection of PGF2 alpha on days 6 or 7 (0 hr) of the estrous cycle. Ewes received 0 or 1 mg CGS per kg BW i.v. every 8 hr from 0 to 40 hr. Ovulation was induced with hCG at 36 hr. CGS reduced jugular (P < .001) and vena caval (P < .001) concentrations of E2, prevented an endogenous surge of LH (P < .05) and increased (P < .001) concentrations of FSH. All ewes had ovulated a marked follicle by 72 hr, but onset of the luteal phase, as assessed by concentrations of P4, was delayed (P < .01) in ewes receiving CGS. Delayed luteal phases were not solely attributable to the presence of new CL or to luteinization of follicular cysts. When data were aligned according to the day ewes were observed in estrus, profiles of P4 did not differ with treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
进行了三项实验，以研究雌二醇 - 17β（E2）浓度降低对随后绵羊黄体（CL）寿命和功能的影响。在实验1中，从10只母羊收集52个卵泡，分别置于含有0或0.01微居里3H - 雄烯二酮（10纳克；3H - A）以及0、10⁻¹¹、10⁻⁹、10⁻⁷或10⁻⁵摩尔非甾体芳香化酶抑制剂CGS16949A（CGS）的单独培养液中。分泌到培养液中的E2浓度以及通过3H - A形成3H - 水估算的雌激素合成量，在10⁻⁵和10⁻⁷摩尔CGS作用下降低（P < 0.01），但10⁻⁹或10⁻¹¹摩尔CGS时未降低。在实验2中，在发情周期第5至10天（0小时）给24只母羊注射PGF2α诱导黄体溶解。母羊在 - 12、0、12和24小时静脉注射每千克体重0、0.5、1.0、2.0或4.0毫克CGS，并在36小时注射排卵剂量的hCG。在所有测试剂量下，CGS使颈静脉（P < 0.001）和腔静脉（P < 0.001）E2浓度在8至10小时内降低，但在下一次注射时已恢复到与对照母羊相似的水平。促黄体生成素（LH）激增时对照和处理母羊的E2浓度相似。在随后的黄体期，对照和处理母羊的孕酮（P4）浓度相似。因此，卵泡期E2的短暂降低对随后的黄体期无害。在实验3中，在发情周期第6或7天（0小时）给18只母羊注射PGF2α诱导黄体溶解。母羊从0至40小时每8小时静脉注射每千克体重0或1毫克CGS。在36小时用hCG诱导排卵。CGS降低颈静脉（P < 0.001）和腔静脉（P < 0.001）E2浓度，阻止内源性LH激增（P < 0.05）并增加（P < 0.001）促卵泡素（FSH）浓度。所有母羊在72小时时都有一个明显的卵泡排卵，但接受CGS的母羊中，根据P4浓度评估的黄体期开始延迟（P < 0.01）。黄体期延迟并非完全归因于新黄体的存在或卵泡囊肿的黄素化。当根据母羊发情观察日对齐数据时，P4曲线在不同处理间无差异。（摘要截断于400字）
