FACTORS CONTRIBUTING TO THE FORMATION OF EXPERIMENTALLY-INDUCED OVARIAN CYSTS IN PREPUBERTAL GILTS

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 appeara nce on nonmanipulated ovaries. In contrast, cysts did not form after m anipulation in luteal phase gilts. In the present experiment, daily ad ministration of 50 mg progesterone to prepubertal gilts treated with P MSG and hCG established luteal phase concentrations of progesterone bu t did not lessen the incidence of manipulated-induced cysts. Number of cysts formed was associated with the number of follicles greater-than -or-equal-to 5 mm at manipulation, which was inversely related to seru m concentrations of progesterone. Number of receptors for LH/hCG in fo llicular tissues did not differ between manipulated and nonmanipulated ovaries but was greater in granulosa (P<.05) and theca (P<.08) from f ollicles with diameters greater-than-or-equal-to 7 mm compared to 5 an d 6 mm. Contents of estradiol, androstenedione, testosterone, progeste rone and prostaglandins E2 and F2alpha in follicular fluid, granulosa and theca were not different between follicles greater-than-or-equal-t o 5 mm destined to form cysts or CL. Exogenous prostaglandin E2 or F2a lpha given during follicular development failed to induce cysts. Profi les of progesterone and estradiol in peripheral serum and duration of luteal phase concentrations of progesterone were not different for gil ts with induced cysts and gilts with CL. In conclusion, manipulation o f follicles resulted in a failure to ovulate. Subsequent formation of cysts did not result from or result in a loss of steroidogenic functio n or the ability to bind LH to follicular receptors. These results dem onstrate that the mechanism for ovulation is independent of other foll icular processes, since ovulation can be disrupted without altering fo llicular steriodogenesis or subsequent luteinization.