title: Prostaglandin E(1) inhibits abnormal follicle rupture and restores ovulation in indomethacin-treated rats.
abstract: In the presence of indomethacin, an inhibitor of prostaglandin (PG) synthesis, the gonadotropin surge induces abnormal follicle rupture at the basolateral follicle sides, thus preventing effective ovulation in rats. This study was undertaken to analyze whether exogenous prostaglandin administration can overcome the antiovulatory action of indomethacin. Cycling rats were treated with vehicle (olive oil) or indomethacin (1 mg/rat) on the morning of proestrus. Rats treated with indomethacin were injected with different doses (50, 250, or 500 micro g/rat) of PGE(1), PGE(2), PGF(2alpha), or vehicle (saline) at 1900 h in proestrus. The ovulatory response was analyzed on the morning of estrus by evaluating follicle rupture and the location of the oocytes in serially sectioned ovaries. The number of oocytes in the oviducts was also counted in rats treated with the highest prostaglandin doses. In indomethacin-treated rats, most newly formed corpora lutea showed abnormal follicle rupture at the basolateral sides. In addition, invasion of the ovarian stroma and blood and lymphatic vessels by granulosa cells and follicular fluid was observed. Prostaglandins of the E series, and especially PGE(1), inhibited abnormal follicle rupture and restored ovulation, although the number of oocytes in the oviducts were significantly decreased. PGF(2alpha) was only partially effective in inhibiting abnormal follicle rupture and restoring ovulation. These data suggest that prostaglandins of the E series, and particularly PGE(1), play a crucial role in ovulation by determining the targeting of follicle rupture at the apex, thus allowing release of oocytes to the periovarian space.
authors.affiliation: Department of Cell Biology, Physiology and Immunology, School of Medicine, University of Cordoba, Spain. bc1galuf@uco.es
authors.forename: Francisco
authors.initials: F
authors.lastname: Gaytán
authors.forename: Esteban
authors.initials: E
authors.lastname: Tarradas
authors.forename: Carmen
authors.initials: C
authors.lastname: Bellido
authors.forename: Concepción
authors.initials: C
authors.lastname: Morales
authors.forename: José Eugenio
authors.initials: JE
authors.lastname: Sánchez-Criado
mesh_terms: D000527:Alprostadil / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D003338:Corpus Luteum / Q000187:drug effects; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology*; D015237:Dinoprost / Q000008:administration & dosage; D015232:Dinoprostone / Q000008:administration & dosage; D005260:Female; D007213:Indomethacin / Q000494:pharmacology*; D009865:Oocytes / Q000502:physiology; D006080:Ovarian Follicle / Q000187:drug effects*; D010060:Ovulation / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D016861:Cyclooxygenase Inhibitors; D015237:Dinoprost; D000527:Alprostadil; D015232:Dinoprostone; D007213:Indomethacin