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首页> 外文期刊>American Journal of Physiology >Platelet-activating factor may act as an endogenous pulse generator for sheep of luteolytic PGF2alpha release.
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Platelet-activating factor may act as an endogenous pulse generator for sheep of luteolytic PGF2alpha release.

机译：血小板活化因子可能充当黄体溶解性PGF2α释放绵羊的内源性脉冲发生器。

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摘要

Pulsatile release of uterine prostaglandin F2alpha (PGF2alpha) induces luteolysis in ruminants. However, the mechanism(s) that initiates and maintains luteolysis has not been defined. The present study tested the hypothesis that the endogenous PGF2alpha pulse generator is uterine-derived platelet-activating factor (PAF). Ovariectomized ewes were given exogenous progesterone (P), estradiol (E), or both (P+E, mimicking the normal luteal phase). Only ewes treated with steroids released PAF into the uterine lumen and had increased PAF:acetylhydrolase activity in the uterine lumen. Steroid treatment also influenced the capacity of the uterus to release PGF2alpha in response to exogenous PAF. PAF infusion did not affect plasma PGF2alpha metabolite (PGFM) levels in control (no steroid treatment) ewes but increased plasma PGFM levels in P+E ewes (P < 0.001) and ewes treated with P or E alone (P < 0.05). Infusion of PAF followed by or coincident with oxytocin (OT) acted in a synergistic manner to increase plasma PGFM levels. Repeated infusion of PAF into the uterus at 1-h intervals induced tachyphylaxis of the PGFM response to PAF; however, sensitivity of the uterus to PAF returned spontaneously by the 6th h. Interferon-tau (IFN-tau) inhibits pulsatile release of PGF2alpha during pregnancy to prevent luteolysis. Exogenous recombinant ovine IFN-tau (50 microgram) inhibited the uterine response to PAF alone or the combined effects of PAF and OT. These results indicate that uterine PAF fulfills many of the criteria for an endogenous PGF2alpha pulse-generator: steroid induction of PAF production and uterine responsiveness to PAF-induced release of PGF; synergistic stimulation of PAF-induced PGF release by OT; inhibition of PAF effects by IFN-tau; and PAF's ability to induce pulses of PGF with a periodicity during a period of chronic exposure of the uterus to PAF.
机译：子宫前列腺素F2alpha（PGF2alpha）的脉冲释放导致反刍动物发生黄体溶解。然而，尚未定义引发和维持黄体溶解的机制。本研究检验了内源性PGF2alpha脉冲发生器是子宫衍生的血小板活化因子（PAF）的假设。卵巢切除的母羊接受外源孕酮（P），雌二醇（E）或两者皆用（P + E，模仿正常的黄体期）。只有用类固醇处理过的母羊才能将PAF释放到子宫腔中，并且子宫腔中的PAF：乙酰水解酶活性增加。类固醇治疗还影响子宫释放PGF2α的能力，以响应外源性PAF。 PAF输注不会影响对照组（未经类固醇处理）母羊的血浆PGF2α代谢产物（PGFM）水平，但会增加P + E母羊（P <0.001）和单独用P或E处理的母羊的血浆PGFM水平（P <0.05）。在催产素（OT）或与之同时发生时，PAF的输注以协同方式增加血浆PGFM水平。以1小时间隔将PAF反复输注到子宫中会导致PGFM对PAF的反应发生速激反应;然而，子宫对PAF的敏感性在第6小时后自动恢复。干扰素-tau（IFN-tau）在怀孕期间抑制PGF2alpha的脉动释放，以防止黄体溶解。外源重组绵羊IFN-τ（50微克）抑制子宫对单独的PAF或PAF和OT联合作用的反应。这些结果表明子宫PAF满足内源性PGF2α脉冲发生器的许多标准：类固醇诱导PAF产生和子宫对PAF诱导的PGF释放的反应; OT对PAF诱导的PGF释放的协同刺激; IFN-τ抑制PAF作用;和PAF在子宫长期暴露于PAF期间周期性地诱发PGF脉冲的能力。

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