Mellin T N, Busch R D
Prostaglandins. 1976 Aug;12(2):303-17. doi: 10.1016/0090-6980(76)90123-4.
A series of experiments were conducted to evaluate the effects of mode and frequency of administration and estrous cycle stage on the response of the cycling ewe to PGF2alpha. The effects of dexamethasone, arachadonic acid and prostaglandin synthetase inhibitors on estrous cycle length and plasma progesterone levels were also determined. Intramuscular administration of 5 or 10 mg of PGF2alpha, on days 8 and 9 after estrus (5 ewes/group), significantly (p less than .01) shortened the mean length of the estrous cycle and the interval from the end of treatment to estrus. Mean plasma progesterone levels, 24 hours after initial injection, were significantly (p less than .01) lowered. When administered on day 8 only, these doses were considerably less effective in shortening estrous cycle length or lowering plasma progesterone levels. Intravaginal administration of PGF2alpha, by polyurethane tampon, was also largely ineffective. Treatment of ewes with 10 mg of PGF2alpha, by polyurethanetampon, was also largely ineffective. Treatment of ewes with 10 mg of PGF2alpha i.m., on days 3 and 4 of the estrous cycle, resulted in a return to estrus in 2 days in 25% of the treated animals. Plasma progesterone levels of PGF2alpha-treated ewes were significantly lower than controls on the second, third and fourth days after the start of dosing. It would appear that PGF2alpha exerts a retarding effect on developing CL functionality. The prostaglandin synthetase inhibitors, aspirin, flufenamic acid and 1-p-chlorobenzylidene-2-methyl-5-methoxy-3-indenylacetic acid, were administered orally or parenterally for 16 days beginning on day 8 of the estrous cycle. These compounds failed to prolong estrous cycle length. Parenteral administration of dexamethasone did not result in PGF2alpha release in the cycling ewe, at least not in quantities sufficient to induce luteolytis. The prostaglandin precursor, arachadonic acid, also was not luteolytic when given parenterally to cycling ewes.
进行了一系列实验，以评估给药方式、频率和发情周期阶段对处于发情周期的母羊对前列腺素F2α（PGF2α）反应的影响。还测定了地塞米松、花生四烯酸和前列腺素合成酶抑制剂对发情周期长度和血浆孕酮水平的影响。在发情后第8天和第9天，对5只母羊/组肌肉注射5或10毫克PGF2α，显著（p小于0.01）缩短了发情周期的平均长度以及从治疗结束到发情的间隔时间。初次注射后24小时，平均血浆孕酮水平显著（p小于0.01）降低。仅在第8天给药时，这些剂量在缩短发情周期长度或降低血浆孕酮水平方面效果要差得多。通过聚氨酯棉塞经阴道给药PGF2α也基本无效。在发情周期的第3天和第4天，对母羊肌肉注射10毫克PGF2α，25%的治疗动物在2天内恢复发情。在给药开始后的第二、第三和第四天，接受PGF2α治疗的母羊的血浆孕酮水平显著低于对照组。看来PGF2α对发育中的黄体功能有抑制作用。从发情周期的第8天开始，口服或非肠道给予前列腺素合成酶抑制剂阿司匹林、氟灭酸和1-对氯苄叉基-2-甲基-5-甲氧基-3-茚满乙酸16天。这些化合物未能延长发情周期长度。非肠道给予地塞米松不会导致处于发情周期的母羊释放PGF2α，至少释放量不足以诱导黄体溶解。前列腺素前体花生四烯酸经非肠道给予处于发情周期的母羊时也没有溶黄体作用。
