The study demonstrates that misoprostol as well as IMN induces morphological changes and inflammatory events of the cervix. Changes of the collagen network were more pronounced in samples obtained from women treated with misoprostol compared to IMN.

A model for in vitro perfusion of the isolated rat ovary was developed. In the luteinized ovaries of PMSG treated rats the relationship between perfusion flow and progesterone production was evaluated. A positive correlation was found indicating that a high blood flow rate may be necessary for an optimal secretion of progesterone from the fully developed corpus luteum in the rat. Also the effects of a continuous exposure of LH on ovarian cyclic AMP and progesterone release was studied. A rapid and sustained increase in both cyclic AMP and progesterone release was seen and this release tended to have episodic pattern with elevations occurring at intervals between 30 and 90 min following LH. Experiments in several species (rabbit, Janson & Albrecht 1975; guinea-pig, Hossainetal. 1979; rat, Pang & Behrman 1979) have indicated that the fully functional corpus luteum (CL) receives more than 80% of the total ovarian flow. Furthermore, these studies show that the CL is one of the most abundantly perfused tissues in the body. The lack of a significant number of arterio-venous shunts within the CL (Janson et al. 1983) indicates that the luteal flow is a capillary flow. The functional sig¬ nificance of its high magnitude still remains ob¬ scure. Since the main function of the CL is produc¬ tion of progesterone it may be speculated to which extent this production rate is dependent on a high luteal flow. Recent investigations in vivo in the rabbit strongly indicate a positive correlation be¬ tween the blood flow and progesterone production in the fully developed CL (Janson et al. 1981). In these experiments, the luteal blood flow was meas¬ ured indirectly with radioactive microspheres and was correlated to the release of progesterone into the ovarian vein.In the search for a simplified model for direct studies of the relationship between capillary flow and progesterone synthesis we have developed an in vitro perfusion model of the isolated rat ovary. The additional aim of the present study was to evaluate this perfusion model from a morphologi¬ cal and functional point of view. Material and MethodsAnimaL· Immature female rats of the Sprague-Dawley strain (Anticimex Ltd., Sweden) were housed under controlled conditions with 14 h light and 10 h dark and fed a standard diet of pellets and water ad libitum. In the morning of day 26 of life the rats were given a single dose of 8 to 10 IU pregnant mare serum gonadotrophin (PMSG, Sigma Co., USA) sc. This resulted in an endo¬ genous LH surge 2 days later and ovulation on the morning of the next day (for references, see Khan 1979). The mean weight of the unperfused ovary was 23 mg and the mean number of CL was 8. Perfusions were carried out 5 days after spontaneous ovulation. Surgical techniqueThe animals were anaesthetized with sodium pentobarbitone (Mebumal vet., ACO, Sweden), 40 mg/kg, ip. The abdomen was opened through a midline incision and the gut covering the lumbar aorta was cut free and put aside. Following ligation of the renal vessels on both sides, the kidneys were rem...

No abstract

Five ovaries from four postmenopausal women undergoing bilateral oophorectomy for benign conditions were prepared for vascular perfusion for 1 to 5 hours in a recirculating system containing oxygenized (5% CO2 + 95% O2) synthethic bicarbonate buffered medium (Medium 199 + 4% bovine serum albumin + antibiotics). Two histologically normal ovaries released measurable amounts of progesterone into the medium. One ovary, containing a simple cyst, released progesterone into the perfusate, and this release was further increased after the addition of hCG at a concentration of 10 IU/ml. A perfused cystadenofibroma released cAMP, progesterone, estradiol and testosterone into the perfusion medium with an augmented release of cAMP, estradiol and testosterone after the addition of hCG. hCG also had a stimulating effect on the release of prostanoids from this tumour. Fluid from tumour cysts, obtained prior to perfusion, contained measurable levels of gonadotrophins, steroids and prostanoids. The isolated perfused ovary model may provide a tool for further exploration of endocrine and oncological aspects of the postmenopausal ovary.

Introduction Mitotane is an adrenolytic drug that is used as an adjuvant to treat adrenocortical carcinoma. This study aimed to evaluate the clinical course and pathogenetic mechanisms underlying ovarian cyst formation in women of reproductive age diagnosed with adrenocortical carcinoma and being treated with mitotane as an adjuvant to surgery. Material and methods Five women presented with stage III‐IV adrenocortical carcinoma and ovarian cyst formation during mitotane treatment. The clinical course of the disease was followed during and after treatment. The effects of mitotane on progesterone production and cell proliferation were studied in cultured human ovarian granulosa cells. Results Computed tomography and vaginal ultrasonography during mitotane treatment repeatedly demonstrated ovarian cysts of varying size without solid intralocular structures. Two women became amenorrheic during the treatment period. After mitotane cessation, the ovarian cysts disappeared and normal menstrual cycles resumed. One woman had an uncomplicated pregnancy two years after mitotane treatment. In one woman, who underwent salpingo‐oophorectomy, histological analysis demonstrated benign ovarian cysts. Mitotane impeded the synthesis of progesterone, reduced the stimulatory effect of gonadotropins on progesterone formation, and reduced labeling with [3H]thymidine in cultured granulosa cells. Conclusions Therapeutic concentrations of mitotane are associated with the formation of benign ovarian cysts and amenorrhea. Mitotane‐induced suppression of ovarian steroidogenesis and impediment of the proliferative capacity of steroid‐producing cells are suggested potential pathogenetic mechanisms underlying mitotane‐induced ovarian dysfunction and cyst development. Mitotane treatment does not compromise future ovarian function.