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

Diane M. Duffy, Richard Stouffer

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    91 Citations (Scopus)

    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.

    Original languageEnglish (US)
    Pages (from-to)2825-2831
    Number of pages7
    JournalHuman Reproduction
    Volume17
    Issue number11
    StatePublished - Nov 1 2002

    Fingerprint

    Cyclooxygenase Inhibitors
    Corpus Luteum
    Macaca mulatta
    Oocytes
    Indomethacin
    Rupture
    Dinoprostone
    Prostaglandin Antagonists
    Ovary
    Primates
    Follicular Fluid
    Injections
    Luteal Phase
    Ovulation
    Serum
    Prostaglandins
    Haplorhini
    Progesterone
    Estradiol
    Estrogens

    Keywords

    • Follicle rupture
    • Ovary
    • Ovulation
    • Prostaglandin

    ASJC Scopus subject areas

    • Physiology
    • Developmental Biology
    • Obstetrics and Gynecology
    • Reproductive Medicine

    Cite this

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    title = "Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without alteration of normal luteal function in rhesus monkeys",
    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.",
    keywords = "Follicle rupture, Ovary, Ovulation, Prostaglandin",
    author = "Duffy, {Diane M.} and Richard Stouffer",
    year = "2002",
    month = "11",
    day = "1",
    language = "English (US)",
    volume = "17",
    pages = "2825--2831",
    journal = "Human Reproduction",
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    TY - JOUR

    T1 - Follicular administration of a cyclooxygenase inhibitor can prevent oocyte release without alteration of normal luteal function in rhesus monkeys

    AU - Duffy, Diane M.

    AU - Stouffer, Richard

    PY - 2002/11/1

    Y1 - 2002/11/1

    N2 - 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.

    AB - 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.

    KW - Follicle rupture

    KW - Ovary

    KW - Ovulation

    KW - Prostaglandin

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