TY - JOUR
T1 - Do prostaglandins lead to ovulation in the rabbit by stimulating proteolytic enzyme activity?
AU - Miyazaki, T.
AU - Katz, E.
AU - Dharmarajan, A. M.
AU - Wallach, E. E.
AU - Atlas, S. J.
N1 - Funding Information:
Received August 28, 1990; revised and accepted February 14, 1991. * Supported by National Institute of Child Health and Human Development HD-19430, The Population Center Grant HD 06268, SmithKline Beecham Fellowship (T.M.), The Rockefeller Foundation (A.M.D.), and The Lillian and Mitchell Duberstein Foundation. t Presented, in part, at the 44th and 45th Annual Meetings of The American Fertility Society, Atlanta, Georgia, October 10 to 13, 1988 and San Francisco, California, November 13 to 16, 1989. :j: Present address: The University of Maryland, Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology, Baltimore, Maryland. § Reprint requests: Edward E. Wallach, M.D., Department of Gynecology and Obstetrics, Johns Hopkins Medical Institutions, 600 N. Wolfe Street, Houck 264, Baltimore, Maryland 21205.
PY - 1991
Y1 - 1991
N2 - Objective: To determine if prostaglandins (PGs) have a direct effect on the ovarian proteolytic enzyme system by examining ultrastructure of the follicle wall and the microvasculature in the presence and absence of indomethacin and by using the isolated perfused rabbit ovary. Design: Nine hours after administration of human chorionic gonadotropin (hCG) or hCG plus indomethacin, follicles were removed and processed for scanning and transmission electron microscopy. Isolated perfused rabbit ovaries were induced to ovulate with PGF(2α) (100 ng/mL) in the presence and absence of tranexamic acid (0.1, 1.0, or 10 mM), a plasminogen activator inhibitor. Results: The addition of indomethacin to hCG inhibited ovulation and production of PGs without affecting the follicular microvasculature. However, the changes in follicle wall architecture were less pronounced after treatment with indomethacin. Ovulatory efficiency in response to PGF(2α) (the percent of follicles > 1.5 mm that ovulate) was significantly reduced (P < 0.01) by 10 mM tranexamic acid. Conclusions: These results suggest that PGs induce follicular rupture by activation of proteolytic enzymes located in the follicle wall.
AB - Objective: To determine if prostaglandins (PGs) have a direct effect on the ovarian proteolytic enzyme system by examining ultrastructure of the follicle wall and the microvasculature in the presence and absence of indomethacin and by using the isolated perfused rabbit ovary. Design: Nine hours after administration of human chorionic gonadotropin (hCG) or hCG plus indomethacin, follicles were removed and processed for scanning and transmission electron microscopy. Isolated perfused rabbit ovaries were induced to ovulate with PGF(2α) (100 ng/mL) in the presence and absence of tranexamic acid (0.1, 1.0, or 10 mM), a plasminogen activator inhibitor. Results: The addition of indomethacin to hCG inhibited ovulation and production of PGs without affecting the follicular microvasculature. However, the changes in follicle wall architecture were less pronounced after treatment with indomethacin. Ovulatory efficiency in response to PGF(2α) (the percent of follicles > 1.5 mm that ovulate) was significantly reduced (P < 0.01) by 10 mM tranexamic acid. Conclusions: These results suggest that PGs induce follicular rupture by activation of proteolytic enzymes located in the follicle wall.
UR - http://www.scopus.com/inward/record.url?scp=0025865834&partnerID=8YFLogxK
U2 - 10.1016/S0015-0282(16)54372-6
DO - 10.1016/S0015-0282(16)54372-6
M3 - Article
C2 - 2037112
AN - SCOPUS:0025865834
SN - 0015-0282
VL - 55
SP - 1183
EP - 1188
JO - Fertility and Sterility
JF - Fertility and Sterility
IS - 6
ER -