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母羊妊娠早期胚胎抗溶黄体活性的相关方面。

Aspects of the antiluteolytic activity of the conceptus during early pregnancy in ewes.

作者信息

Lacroix M C, Kann G

出版信息

J Anim Sci. 1986 Nov;63(5):1449-58. doi: 10.2527/jas1986.6351449x.

Abstract

Experiments were undertaken to determine whether the conceptus renders a corpus luteum resistant to the luteolytic action of prostaglandin F2 alpha (PGF2 alpha), and modulates release of this prostaglandin by the uterus of early pregnant ewes. Prostaglandin F2 alpha was luteolytic when administered to indomethacin-treated ewes on d 10 and 11 of the estrous cycle. The same PGF2 alpha treatment was not luteolytic when applied on d 19 and 20 of pregnancy in ewes treated with indomethacin. Pulsatile release of PGF2 alpha (measured by 15-keto-13,14-dihydro PGF2 alpha-PGF2 alpha plasma level, PGFM) was observed between d 14 and 16 of the cycle but not during the same period of pregnancy. Ablation of the conceptus on d 17 resulted in progressive restoration of PGFM surges and subsequent luteolysis. Estradiol-17 beta (E2-17 beta) administration on d 12 of the cycle induced earlier PGFM surges and luteal regression. The same E2-17 beta treatment administered on d 14, 19 and 33 of pregnancy failed to induced PGFM pulses and luteolysis. In the absence of the conceptus (surgical ablation), E2-17 beta treatment was luteolytic (PGFM surges) on d 17 but not on d 33. We conclude that the conceptus controls the amount and pattern of PGF2 alpha released by the uterus, as well as the sensitivity of the uterus to E2-17 beta as early as d 14 of pregnancy. Simultaneously, an embryonic protective effect takes place at the luteal level.

摘要

开展实验以确定孕体是否使黄体对前列腺素F2α(PGF2α)的溶黄体作用产生抗性,并调节早孕母羊子宫中这种前列腺素的释放。在发情周期的第10天和第11天,对用吲哚美辛处理的母羊施用PGF2α时具有溶黄体作用。在用吲哚美辛处理的母羊妊娠第19天和第20天进行相同的PGF2α处理时则没有溶黄体作用。在周期的第14天至16天观察到PGF2α的脉冲式释放(通过15-酮-13,14-二氢PGF2α - PGF2α血浆水平,即PGFM来测定),但在妊娠同期未观察到。在第17天切除孕体导致PGFM峰逐渐恢复并随后黄体溶解。在周期的第12天施用雌二醇-17β(E2-17β)诱导更早的PGFM峰和黄体退化。在妊娠第14天、19天和33天进行相同的E2-17β处理未能诱导PGFM脉冲和黄体溶解。在没有孕体的情况下(手术切除),E2-17β处理在第17天具有溶黄体作用(PGFM峰),但在第33天没有。我们得出结论,早在妊娠第14天,孕体就控制子宫释放PGF2α的量和模式,以及子宫对E2-17β的敏感性。同时,在黄体水平发生胚胎保护作用。

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