Lack of fluctuation in growth hormone secretion during early sleep in early and midmenstrual cycle.
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Pain threshold to mechanical stimulus was determined in 140 subjects comprising of healthy volunteers of both sexes and of different ages, females taking oral contraceptives and bilaterally oopherectomised females. Pain threshold was observed to be low in oopherectomised females, boys and girls and intermediate in healthy males. It was high in menstruating females aged 18-21 years. There was a marked fluctuation in pain threshold in menstruating females. It was low at menstrual phase. In females taking oral contraceptives it was high at pre and midmenstrual phases. In females not taking oral contraceptives it was low at pre-menstrual and high as midmenstrual phases.
The repeated observation of a fall in serum enzymes at midmenstrual cycle in an untreated patient with primary biliary cirrhosis stimulated a study of estrogen administration in five patients with primary biliary cirrhosis. One patient was premenopausal, one patient was postmenopausal and three had had oophorectomy. After 2 weeks of ethinyl estradiol, AST was under 100 IU per dl in all and had decreased by 50% or more in 4 of 5 patients. gamma-glutamyltransferase and alkaline phosphatase fell by 50 and 30% or more, respectively, in all patients. The decreases in serum enzymes were statistically significant in all patients for gamma-glutamyltransferase, in 4 of 5 for AST and in 3 of 5 for alkaline phosphatase. One patient developed increased icterus leading to withdrawal of estradiol. Withdrawal of estradiol was followed by return toward control values over variable periods, usually 1 to 4 weeks. Repeated courses of estradiol reproduced these enzyme changes. These observations indicate that estradiol in the doses used (0.05 mg per day) reversibly lowers serum enzyme values in biliary cirrhosis. The mechanism of the effect is unexplained, but an immune system alteration may be responsible.
OBJECTIVES: The goal of this study was to investigate the mechanism of reduced vasoconstrictor sensitivity to norepinephrine in women compared with men. BACKGROUND: beta2-adrenergic agonists such as albuterol dilate forearm resistance vessels, partly by activating the L-arginine/nitric oxide pathway. Norepinephrine (which acts as beta- as well as alpha-adrenergic receptors) causes less forearm vasoconstriction in women than it does in men. This could be explained by a greater sensitivity to beta2-receptor stimulation in women than in men. METHODS: Forearm blood flow was measured by venous occlusion plethysmography in healthy women (days 10 to 14 of the menstrual cycle) and in men. Drugs were administered via the brachial artery in three separate protocols: albuterol +/- NG-monomethyl-L-arginine (an inhibitor of nitric oxide synthase); substance P, nitroprusside and verapamil (control vasodilators); norepinephrine (+/- propranolol, a beta-adrenergic receptor antagonist). RESULTS: Vasodilator responses to albuterol were greater in women than they were in men (p = 0.02 by analysis of variance). NG-monomethyl-L-arginine reduced these similarly in men and women. Responses to control vasodilators were less in women than they were in men (each p < 0.05). Norepinephrine caused less vasoconstriction in women than it did in men (p = 0.02). Propranolol did not influence basal flow in either gender nor responses of men to norepinephrine but increased vasoconstriction to each dose of norepinephrine in women (p < 0.0001 for interaction between gender and propranolol). Responses to norepinephrine coinfused with propranolol were similar in men and women. CONCLUSIONS: Stimulation of beta2-adrenergic receptors causes greater forearm vasodilation in premenopausal women, at midmenstrual cycle, than it does in men. This is sufficient to explain why vasoconstriction to brachial artery norepinephrine is attenuated in such women.
Renin is classically considered to be an enzyme that is synthesized by the kidneys and secreted into the circulation where it affects angiotensin production. We review here recent evidence that suggests the existence of an extra-renal renin system, the ovarian prorenin-renin-angiotensin system, which may be linked to reproductive function. Prorenin, the inactive form of the enzyme renin, is present in the fluid of mature human ovarian follicles in extremely high concentrations; however, only 1 per cent of the renin in follicular fluid is in the active form. Plasma prorenin increases about 2-fold at midmenstrual cycle at the time of the LH surge, and the peak of prorenin is sustained for about 2 days. No change in plasma active renin levels occurs at this time. Administration of hCG to women whose ovaries have been stimulated with gonadotropins results in much higher plasma prorenin levels and the height of prorenin response is directly related to the number of mature follicles. Plasma prorenin also increases 10-fold during the early stages of pregnancy. It begins to rise on days 8 to 12 after embryo transfer, in parallel with the rise in endogenous hCG. The ovaries are the apparent source of the increase in plasma prorenin in early pregnancy since no such increase in prorenin occurred in a woman with ovarian failure who conceived after receiving a donor egg. These results suggest that prorenin is synthesized and secreted by the mature ovarian follicle and by the corpus luteum in response to LH/hCG. They also suggest that an ovarian renin system exists that is regulated by changes in prorenin.(ABSTRACT TRUNCATED AT 250 WORDS)
Two women with the Prader-Labhart-Willi syndrome are presented. The gonadotropin response to LH-RH administration was studied prior to, immediately following, and 6 months after a 6-week trial of clomiphene citrate, 200 mg per day for 21 days in divided doses, followed by 100 mg for 21 days in divided doses, followed by 100 mg per day for 14 days in divided doses, and followed by 50 mg per day in a single dose for an additional 14 days. During therapy, the basal gonadotropin and estradiol concentrations rose from prepubertal levels to those of mature women in midmenstrual cycle. However, 6 months after cessation of treatment, the basal gondadotropin and estradiol levels had returned to the prepubertal range. The initial response to LH-RH in the 2 patients differed in that one was clearly prepubertal and the other indistinguishable from the broad range of the adult normal response. The LY and FSH responses to LH-RH administration was greater after 6 weeks of clomiphene citrate therapy than they were either before (both patients) or 6 months after treatment (1 patient). We conclude that there is heterogeneity in the response to LH-RH administration in the Prader-Labhart-Willi Syndrome, just as there is in other syndromes of hypogonadotropic hypogonadism. A normal adult response of gonadotropins to the administration of LH-RH was acheived during clomiphene citrate therapy.
The menstrual cycle has been reported to alter pain perception but the patterns differ among studies. It has been reported that estrogens may influence somatic sensory processes. The present aim was to investigate whether the perception of pain varies by phases of the menstrual cycle. 20 women with chronic low pain volunteered to participate and were asked to rate their pain each day during three successive menstrual cycles. The menstrual cycle was divided into four and five phases to be able to compare results. Analysis showed there were phase differences in pain ratings during the menstrual cycle. Regardless of whether the menstrual cycle was divided into four or five phases, women rated pain significantly higher in the menstrual and premenstrual phases than in the midmenstrual and ovulatory phases. This is consistent with other studies showing less pain sensitivity during phases of the menstrual cycle associated with high estrogen. Women with high pain frequency reported more frequently a passive coping style and catastrophizing thoughts.
The relationship between the time in the menstrual cycle when a TCu-200 or Cu-7-200 is inserted and subsequent IUD-related events was evaluated. For women who had either TCus or Cu-7s inserted, the pregnancy, expulsion and medical removal rates were similar for insertions performed at any time of the menstrual cycle.
The administration of RU38486 (RU486) in the luteal phase may induce menstruation, but it may not be associated with shedding of the functional layer of the endometrium. This provides an explanation why, in some cases of successful menstrual induction by RU486, pregnancy continues undisturbed. The ability of RU486 to interrupt a very early pregnancy is more likely to be related to its ability to cause shedding of the endometrium than its ability to induce menstruation.
The relation between the use of oral contraceptives and changes in positive and negative affect over the course of the menstrual cycle was studied in 50 women who completed a mood questionnaire daily during their menstrual cycle. Results indicated that users of oral contraceptives experience a higher level of positive affect during the cycle than do non-users. Positive affect scores were significantly higher than negative affect scores in the menstruation, follicular and luteal phases of the cycle. There were no significant differences between the groups and no discernible phasic changes on negative affect. Discussion of these findings centers on their implications concerning the relation between positive affect and oral contraceptives, the support they provide for the independence of positive and negative affect, and future directions for research in this area.
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This study was designed to assess the features and conditions for endometrial bleeding induction with the synthetic antiprogestin and antiglucocorticoid RU 486 during hCG-induced prolongation of the luteal phase. Eighteen healthy, surgically sterilized women and another five women with an intrauterine contraceptive device (IUD) participated. All subjects received hCG which was injected daily in increasing doses (500 to 15,000 IU) from day 9 to day 15 of the luteal phase. Ten subjects received hCG alone, and groups of three to 16 subjects received hCG combined with RU 486 (25, 50, 100, 200 or 400 mg/day). RU 486 administration was commenced on day 12 following the LH surge and given either for 1, 4 or 7 consecutive days. In certain cycles, tamoxifen (20 mg/day) was given for 4 consecutive days with hCG, or with hCG and RU 486. All treatment cycles were separated by one or two resting cycles. Frequent blood samples were taken to monitor the endocrine response. Treatment with hCG alone or with the various combinations of RU 486 produced similar serum levels of oestradiol and progesterone which were equivalent to those observed during early pregnancy. With hCG alone, the onset of bleeding was on day 21-24 after the LH surge, coinciding with the drop in oestradiol and progesterone. With RU 486 doses of 50 mg/day or more, an early bleeding episode almost invariably occurred on day 14-17 after the LH surge in the presence of high circulating steroid levels. In contrast, 25 mg/day RU 486 for 4 days failed to induce this early onset of bleeding in three out of six cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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Healthy, regularly menstruating women were treated with the antiprogesterone RU 486, Mifepristone (Roussel-Uclaf, Romainville, France) during the follicular phase of the cycle. Three women were given 25 mg of RU 486 on days 1 to 14 of the cycle and five received 25 mg on days 1 to 21 of the cycle. Venous blood samples were collected three times per week during a control cycle and during one treatment cycle in each subject. Serum concentrations of estradiol (E2), progesterone (P), and RU 486 were determined by radioimmunoassays. No drug-related side effects and no spotting or bleeding during RU 486 treatment were observed. Menstrual bleeding was delayed by 8.7 +/- 3.8 days (mean +/- SD) after treatment over days 1 to 14 and by 12.6 +/- 3.2 days after treatment over days 1 to 21. During the treatment with RU 486, the serum concentrations of E2 remained low, indicating effective inhibition of folliculogenesis. After cessation of RU 486 treatment, serum E2 levels rose to similar values as in the control cycle, and subsequently serum P concentrations also reached ovulatory levels in six out of the eight volunteers. The results showed that the antiprogesterone RU 486 delayed folliculogenesis and luteinization even at low doses when given during the follicular phase of the menstrual cycle. It is speculated that this property of RU 486 could be utilized in the design of an estrogen-free combined oral contraceptives.
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