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Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without alteration of normal luteal function in rhesus monkeys

Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without... BACKGROUND: Prostaglandins (PG), produced by the follicle just before ovulation, appear to act locally to promote follicle rupture and oocyte release. METHODS: To determine whether administration of PG synthesis inhibitor directly into the primate follicle would prevent ovulatory events, serum estradiol was used to predict the day of the ovulatory LH surge in rhesus monkeys. On the day before or the day of the LH surge, vehicle (n = 9), the PG synthesis inhibitor indomethacin (10−6 or 10−5 mol/l final concentration; n = 8), or 10−5 mol/l indomethacin + 1 μg/ml PGE2 (n = 3) was injected into the follicular fluid of the pre-ovulatory follicle. In some animals, luteal phase estrogen and progesterone were measured in daily serum samples. Other animals were ovariectomized 3 days after follicle injection; ovaries were examined for verification of follicle rupture and oocyte release. RESULTS: Follicle injection of indomethacin [10−6 mol/l (n = 4) or 10−5 (n = 4) mol/l final concentration] or vehicle (n = 6) did not alter luteal function. Examination of serial sections of removed ovaries confirmed follicle rupture and the absence of oocytes in vehicle-injected follicles (n = 3). Trapped oocytes were observed in 4/8 indomethacin-injected follicles, though several ovaries with trapped oocytes had experienced follicle rupture. Oocytes were not detected in the ruptured, luteinizing follicles from indomethacin + PGE2-injected monkeys (n = 3). CONCLUSIONS: Follicular administration of indomethacin can prevent oocyte release without inhibition of follicle rupture or disruption of subsequent luteal function. The ability of PGE2 to prevent indomethacin-induced ovulatory failure suggests a critical role for locally produced PGE2 in the process of oocyte release in primates. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Human Reproduction Oxford University Press

Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without alteration of normal luteal function in rhesus monkeys

Duffy, Diane M.; Stouffer, Richard L.
Human Reproduction , Volume 17 (11) – Nov 1, 2002
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References (26)

Publisher
Oxford University Press
Copyright
© European Society of Human Reproduction and Embryology
ISSN
0268-1161
eISSN
1460-2350
DOI
10.1093/humrep/17.11.2825
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Abstract

BACKGROUND: Prostaglandins (PG), produced by the follicle just before ovulation, appear to act locally to promote follicle rupture and oocyte release. METHODS: To determine whether administration of PG synthesis inhibitor directly into the primate follicle would prevent ovulatory events, serum estradiol was used to predict the day of the ovulatory LH surge in rhesus monkeys. On the day before or the day of the LH surge, vehicle (n = 9), the PG synthesis inhibitor indomethacin (10−6 or 10−5 mol/l final concentration; n = 8), or 10−5 mol/l indomethacin + 1 μg/ml PGE2 (n = 3) was injected into the follicular fluid of the pre-ovulatory follicle. In some animals, luteal phase estrogen and progesterone were measured in daily serum samples. Other animals were ovariectomized 3 days after follicle injection; ovaries were examined for verification of follicle rupture and oocyte release. RESULTS: Follicle injection of indomethacin [10−6 mol/l (n = 4) or 10−5 (n = 4) mol/l final concentration] or vehicle (n = 6) did not alter luteal function. Examination of serial sections of removed ovaries confirmed follicle rupture and the absence of oocytes in vehicle-injected follicles (n = 3). Trapped oocytes were observed in 4/8 indomethacin-injected follicles, though several ovaries with trapped oocytes had experienced follicle rupture. Oocytes were not detected in the ruptured, luteinizing follicles from indomethacin + PGE2-injected monkeys (n = 3). CONCLUSIONS: Follicular administration of indomethacin can prevent oocyte release without inhibition of follicle rupture or disruption of subsequent luteal function. The ability of PGE2 to prevent indomethacin-induced ovulatory failure suggests a critical role for locally produced PGE2 in the process of oocyte release in primates.

Journal

Human Reproduction – Oxford University Press

Published: Nov 1, 2002

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