Ovarian contractility and ovulation.
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Iproniazid, a very specific monoamine oxidase inhibitor, at a dose level of 200 mg/kg body weight induced luteolysis and caused lysis of deciduomata as well as resorption of the established embryos. Exogenous replacement of prolactin, a most consistent stimulant of the endocrine functioning of corpus luteum, or progesterone absolutely reversed the adversity developed following iproniazid injection. Moreover, failure of iproniazid even at a higher dose level in the deviation of the normal sequence of pregnancy after the establishment of placental adolescence strongly tempting to suggest that iproniazid could only show its luteolytic effect when the hypothalamic-pituitary complex is exclusively involved in the maintennance of pregnancy.
The motility and the pharmacological reactivity of the uterine tract of mammals are linked with the ovarian cycle and the gestation. In the birds, the study of general scheme of the hormonal mechanism and the uterine motility involued in the ovulation, the egg formation and the uterine dilatation can be used as an experimental model of the mammalian gestation.
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Although there is general agreement about the polycystic ovary as an anatomic entity, a classic description of an associated syndrome remains elusive. This lack of definition, however, has not impeded clinical investigation. This article focuses on the diagnosis, pathogenesis, hypotheses, and treatment of polycystic ovarian disease.
Endocrinological changes due to the effect of treatment with mono-, bi- and three-phase contraceptive pills taking continuously and occasionally are reviewed. It is established that oral contraceptives based on ovulation inhibition are safe. Less side effects are produced by Ovidon tablets. Continuin and Postinor pills are not safe, and they can produce irregular bleeding. Beside their numerous advances extrauterine pregnancy frequently happens (6.4%). A three-phase preparation is expected to have a reversible effect and lack of a consequent functional infertility. This is improved by hormone level measurements.
Seven patients had autoimmune progesterone dermatitis. The morphological findings illustrate the polymorphous nature of the disease in which urticaria, erythema multiforme, and dyshidrosiform lesions were seen. Recurrence of the eruption five to ten days prior to the menses with spontaneous resolution following the menses was present in all cases. Intradermal skin testing to progesterone was done to confirm the diagnosis. Six of the seven patients has a history of use of artificial progestational hormones prior to the beginning of their eruption. It is postulated that the artificial progesterones may have been the trigger for the development of their autosensitivity. Treatment with conjugated estrogens resulted in remission of the disease in five of the seven cases reported.
In order to determine the pituitary or ovarian site of the anti-gonadotrophic action of prolactin (PRL), ten women with hyperprolactinaemia were studied in the following way: 1) Repeated estimations of PRL, gonadotrophins (LH and FSH), plasma estradiol and progesterone during six weeks of treatment with bromocriptine. 2) Verification of the effects of estradiol benzoate on LH and FSH levels before and after normalisation of prolactin. 3) Exploration of the ovarian response to the administration of human menopausal gonadotrophin. Without it being possible to exclude any direct effect of prolactin on the ovary, it may be affirmed that the hormone decreases the sensitivity of the gonadotrophic cells to the positive feedback mechanism exerted by plasma estradiol.
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In the past, numerous efforts have been made to define risk and protective factors of breast cancer. Among these, pregnancy and lactation have been extensively discussed in connection with breast cancer. Unfortunately, many of the reports on the protective effects of pregnancy and lactation are equivocal; caution needs to be exercised when interpreting the results of a single publication. Development of breast cancer is often preceded by the occurrence of preneoplastic mammary lesions, which may be the result of long-term exposure to estrogens and prolactin. Since endogenous estrogen levels regulate pituitary prolactin secretion to some extent, it has been postulated that a hormonal imbalance exists in early mammary carcinogenesis. Exogenous estrogens directly increase pituitary prolactin secretion. During gestation, greatly increased levels of endogenous sex steroids efficiently stimulate pituitary prolactin secretion; during lactation, the stimulus of suckling is responsible for hyperprolactinemia. However, most studies did not reveal a cause-effect relationship between prolactin levels and enhanced risk of breast cancer. At present, the role of pregnancy and lactation in the development and prognosis of breast cancer is not determined.
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The presence of several hormones in milk occurring either by passive diffusion or by active concentrating mechanism from blood can be of great concern to the neonate. According to Fulkerson [1979] when the clearance rates of the hormones out of blood is considered, this worry is unwarranted. Concerning the steroids, when their levels have been monitored in milk after lactogenesis, the worry for the baby seems to be unfounded. But with the new finding of high level of LH-RH in milk whose concentration far exceeds that of blood, care should be taken to examine in the neonates whether the levels of LH and FSH become disproportionately high and induce the secretion of gonadal steroids at a higher level.
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The menstrual cycle is regulated by a complex hormonal system with positive and negative feedback mechanisms and changes in sensitivity of peripheral tissues. Four concepts appear to be fundamental: -- regular, pulsatile secretion of LHR is necessary to the functioning of the system; -- regulation is to a great extent effected by the pituitary gland in response to changes in ovarian steroid levels; -- changes in ovarian steroid levels are due to regulatory changes in receptivity to pituitary hormones, as well as to variations in enzyme activities; -- at the periphery, changes in hormonal impacts are accompanied by modifications of receptivity to steroid hormones.
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The authors have studied the long-term effects of combined oestrogen-progestogen on the secretion of gonadotrophins and on ovarian function. Estimation of the radio-immune levels of the plasma concentrations of the pituitary luteinizing hormone (LH), of oestradiol (E2), of progesterone (P) and of 20 alpha hydroxyprogesterone (20 alpha OHP) and of testosterone (T) served as a base for this study. A test cycle and 8 cycles in which a combination of 50 micrograms of ethinyl-oestradiol and 0.5 mg of norgestrel were administered were studied in 4 normal volunteer women. A pituitary stimulation test using 50 micrograms of gonadotrophin "releasing factor" (LH-RH) was given during the 7th cycle. Ovarian stimulation using human menopausal gonadotrophins (HMG) was given during the 8th cycle of treatment in 3 of the women and in 3 other subjects. Pituitary secretion of LH and ovarian secretion of E2 and P are partially inhibited. Pituitary response to the injection of LH-RH stays normal but 5 out 6 patients had no response to stimulation by gonadotrophins. These results allow us to conclude that the lowering of production of gonadotrophins during treatment with combination oestrogen and progestagens is responsible for inhibition of ovarian activity, and that there is a delay before the latter respond to stimulation by either endogenous or exogenous gonadotrophins.