title: Factors contributing to the formation of experimentally-induced ovarian cysts in prepubertal gilts.
abstract: Manipulation of an ovary during the follicular phase in cycling gilts or prepubertal gilts treated with PMSG and hCG results in formation of cysts on manipulated ovaries and corpora lutea (CL) of normal appearance on nonmanipulated ovaries. In contrast, cysts did not form after manipulation in luteal phase gilts. In the present experiment, daily administration of 50 mg progesterone to prepubertal gilts treated with PMSG and hCG established luteal phase concentrations of progesterone but did not lessen the incidence of manipulated-induced cysts. Number of cysts formed was associated with the number of follicles > or = 5 mm at manipulation, which was inversely related to serum concentrations of progesterone. Number of receptors for LH/hCG in follicular tissues did not differ between manipulated and nonmanipulated ovaries but was greater in granulosa (P < .05) and theca (P < .08) from follicles with diameters > or = 7 mm compared to 5 and 6 mm. Contents of estradiol, androstenedione, testosterone, progesterone and prostaglandins E2 and F2 alpha in follicular fluid, granulosa and theca were not different between follicles > or = 5 mm destined to form cysts. Profiles of progesterone and estradiol in peripheral serum and duration of luteal phase concentrations of progesterone were not different for gilts with induced cysts and gilts with CL. In conclusion, manipulation of follicles resulted in a failure to ovulate. Subsequent formation of cysts did not result from or result in a loss of steroidogenic function or the ability to bind LH to follicular receptors. These results demonstrate that the mechanism for ovulation is independent of other follicular processes, since ovulation can be disrupted without altering follicular steriodogenesis or subsequent luteinization.
authors.affiliation: Division of Animal and Veterinary Sciences, West Virginia University, Morgantown 26506-6108.
authors.forename: J A
authors.initials: JA
authors.lastname: Hall
authors.forename: E M
authors.initials: EM
authors.lastname: Meisterling
authors.forename: A M
authors.initials: AM
authors.lastname: Benoit
authors.forename: D A
authors.initials: DA
authors.lastname: Cooper
authors.forename: D A
authors.initials: DA
authors.lastname: Coleman
authors.forename: S P
authors.initials: SP
authors.lastname: Lerner
authors.forename: P E
authors.initials: PE
authors.lastname: Lewis
authors.forename: R A
authors.initials: RA
authors.lastname: Dailey
mesh_terms: D000818:Animals; D006063:Chorionic Gonadotropin; D015237:Dinoprost / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis; D004195:Disease Models, Animal; D005260:Female; D015571:Follicular Fluid / Q000737:chemistry; D012739:Gonadal Steroid Hormones / Q000096:biosynthesis; D006064:Gonadotropins, Equine; D006107:Granulosa Cells / Q000378:metabolism; D008183:Luteal Phase / Q000187:drug effects; D010048:Ovarian Cysts / Q000209:etiology / Q000662:veterinary*; D006080:Ovarian Follicle / Q000033:anatomy & histology / Q000187:drug effects / Q000378:metabolism; D011374:Progesterone / Q000096:biosynthesis / Q000494:pharmacology; D011897:Random Allocation; D011974:Receptors, LH / Q000096:biosynthesis; D013552:Swine; D013553:Swine Diseases / Q000209:etiology*; D013799:Theca Cells / Q000378:metabolism
chemical_list: D006063:Chorionic Gonadotropin; D012739:Gonadal Steroid Hormones; D006064:Gonadotropins, Equine; D011974:Receptors, LH; D011374:Progesterone; D015237:Dinoprost; D015232:Dinoprostone